1. Catalog
  2. Nodes
  3. path(MESH:Hemolysis)

path(MESH:Hemolysis)

Equivalencies: 0 | Classes: 0 | Children: 0 | Explore

Entity

Name
Hemolysis
Namespace
MeSH
Namespace Version
20181007
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/01c9daa61012b37dd0a1bc962521ba51a15b38f1/external/mesh-names.belns

Appears in Networks 1

Heme Curation v0.0.1-dev

Mechanistic knowledge surrounding heme

In-Edges 117

a(CHEBI:"desferrioxamine B") decreases path(MESH:Hemolysis) View Subject | View Object

These results suggested that the treatment of DFX reduced the process of hemolysis after ICH, which might be due to alleviating MAC formation. PubMed:27125525

Appears in Networks:
Annotations
MeSH
Cerebral Hemorrhage
Text Location
Results

a(CHEBI:"hydrogen peroxide") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Finally, slower Prx-2 reduction correlated with increased H2O2 (10 lM)-induced hemolysis of day 35 RBC compared with day 7 RBC (Fig. 1D). PubMed:25264713

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
Text Location
Results

a(CHEBI:"iron trichloride") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Analysis of the time course of hemolysis in whole blood revealed a rapid linear increase in Hb levels, peaking 10 min after FeCl3 addition (Fig. 2B), a time course consistent with the rapid hemolysis and vascular injury observed in the ex vivo aortic thrombosis model. PubMed:19276082

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Aorta
Text Location
Introduction

a(CHEBI:"phosphatidyl-L-serine") increases path(MESH:Hemolysis) View Subject | View Object

The abnormal phospholipid membrane asymmetry present in the RBCs of b-thalassaemia and SCD patients, with resultant phosphatidylserine exposure, appears to play a significant role in the aetiology of the observed hypercoagulable state and in the link between haemolysis and thrombosis (Ataga et al, 2007). PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Sickle Cell
MeSH
beta-Thalassemia
Text Location
Review

a(CHEBI:Thrombin) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

However, 6 years later, Heyes and co-workers demonstrated in an experimental study in rats that infusions of thrombin induce DIC accompanied with hemolysis and schistocytosis [89]. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Adenocarcinoma
Text Location
Review

a(CHEBI:argatroban) decreases path(MESH:Hemolysis) View Subject | View Object

Recently, using a rat model of lipopolysaccharide (LPS)-induced systemic inflammation, our own collaboration could show that argatroban (a specific direct thrombin inhibitor and consequently an inhibitor of coagulation) abolishes DIC, schistocyte formation, and hemolysis. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Disseminated Intravascular Coagulation
Text Location
Review

a(CHEBI:eptifibatide) causesNoChange path(MESH:Hemolysis) View Subject | View Object

Interestingly, inhibition of coagulation is capable of diminishing DIC and hemolysis but not antiplatelet therapy—treatment with eptifibatide (an antiplatelet drug of the glycoprotein IIb/IIIa inhibitor class) failed to reduce LPS-induced DIC, schistocyte formation, and hemolysis. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Disseminated Intravascular Coagulation
Text Location
Review

a(CHEBI:glucose) negativeCorrelation path(MESH:Hemolysis) View Subject | View Object

Without sufficient glucose supply, red blood cells will starve and perish and cytoplasmic components will release. Hemolysis will be the consequence [120]. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Disseminated Intravascular Coagulation
Text Location
Review

a(CHEBI:glucose) negativeCorrelation path(MESH:Hemolysis) View Subject | View Object

Recently, our own collaboration could show that moderate glucose supply reduces hemolysis in rats treated with LPS to induce systemic inflammation [121]. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Disseminated Intravascular Coagulation
Text Location
Review

a(CHEBI:heme) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Free heme is generated by intra- and extra-vascular hemolysis or extensive cell damage [14, 15]. PubMed:24464629

Appears in Networks:
Annotations
MeSH
Kidney
Text Location
Introduction

a(CHEBI:heme) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Lysis of red blood cells with consequent increases in free heme most likely caused the increase in HO-1 activity responsible for increased COHb concentrations, which is similar to that observed with circulatory devices [6]. PubMed:24553061

Appears in Networks:
Annotations
Text Location
Discussion

a(CHEBI:heme) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Haemoglobin and haem levels increase in plasma and urine when haptoglobin and haemopexin scavenging mechanisms are saturated during acute or chronic haemolysis. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Plasma
MeSH
Urine
Text Location
Review

a(CHEBI:heme) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

The above-discussed findings provide strong in vivo evidence that high concentrations of ferric Hb(Fe3+) and free heme can accumulate in the renal cortex during hemolysis. PubMed:26794659

Appears in Networks:
Annotations
Cell Ontology (CL)
epithelial cell
MeSH
Kidney Cortex
Text Location
Discussion

a(CHEBI:heme) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

During hemolysis, hemoglobin and heme released from red blood cells promote oxidative stress, inflammation and thrombosis. PubMed:29694434

Appears in Networks:
Annotations
Text Location
Introduction

a(CHEBI:heme) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

In infectious diseases, such as malaria and sepsis, high amounts of cell-free hemoglobin and heme were found [8], suggesting that hemolysis during sepsis and systemic inflammation is of pathophysiological relevance. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
hepatocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

bp(GO:"complement activation") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Activation of the complement system and the formation of MAC resulted in an increased membrane permeability and erythrocyte lysis. PubMed:27125525

Appears in Networks:
Annotations
MeSH
Cerebral Hemorrhage
Text Location
Results

a(CHEBI:lecithin) negativeCorrelation path(MESH:Hemolysis) View Subject | View Object

Already in 1941, Macfarlane and collaborators described hemolysis due to loss of lecithin from the red blood cell membrane in consequence of an infection with Clostridium perfingens [128, 130]. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

a(CHEBI:methemoglobin) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

The above-discussed findings provide strong in vivo evidence that high concentrations of ferric Hb(Fe3+) and free heme can accumulate in the renal cortex during hemolysis. PubMed:26794659

Appears in Networks:
Annotations
Cell Ontology (CL)
epithelial cell
MeSH
Kidney Cortex
Text Location
Discussion

a(HM:"Glucose-6-phosphate dehydrogenase deficiency") increases path(MESH:Hemolysis) View Subject | View Object

Multiple haemolytic disorders and therapeutic interventions produce substantial intravascular haemolysis. Examples include PNH, SCD, thalassaemias, glucose-6-phosphate dehydrogenase (G6PD) deficiency, hereditary spherocytosis and stomatocytosis, pyruvate kinase deficiency, autoimmune haemolytic anaemia, microangiopathies, acute haemolytic transfusion reactions, mechanical circulatory support [e.g., left ventricular assist device (LVAD)/extracorporeal membrane oxygenation (ECMO)], RBC transfusions and infusions of RBC substitutes. These disorders, therapies and procedures are also associated with an increased risk of thrombosis. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Plasma
MeSH
Urine
Text Location
Review

a(HM:"Glucose-6-phosphate dehydrogenase deficiency") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

This common X-linked inherited disorder, characterized by severe intravascular and extravascular haemolysis, is classically triggered by fava bean ingestion or pro-oxidant medications. It causes haemolysis in susceptible individuals and an association with thrombosis was described in multiple case reports (Jewett, 1976; Thompson et al, 2013; Albertsen et al, 2014). PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

a(HM:"fibrin deposition") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

This study further supports the concept that fibrin deposition in the blood vessels as a result of DIC might contribute to red blood cell fragmentation and, in turn, hemolysis [89]. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Disseminated Intravascular Coagulation
Text Location
Review

a(HM:"stored erythrocytes") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Storage is known to result in increased hemolysis which in turn results in loss of NO-signaling, oxidative stress and inflammation post-transfusion. PubMed:26202471

Appears in Networks:
Annotations
Text Location
Discussion

a(HM:"stored erythrocytes") increases path(MESH:Hemolysis) View Subject | View Object

The stored RBCs had approximately 7 times the hemolysis of fresh blood. PubMed:27308950

Appears in Networks:
Annotations
MeSH
Endothelium, Vascular
Text Location
Introduction

a(HM:"stored erythrocytes") increases path(MESH:Hemolysis) View Subject | View Object

Any increase in hemolysis after transfusion of stored RBCs can be attributed to lysis of RBCs during storage or after transfusion (Figure 1B). PubMed:27308950

Appears in Networks:
Annotations
MeSH
Plasma
Text Location
Discussion

a(HM:"stored erythrocytes") increases path(MESH:Hemolysis) View Subject | View Object

Stored RBCs undergo a complex structural and metabolic impairment that includes leakage of hemoglobin from the cells and hemolysis, reduced energy and NO production, formation of toxic products, such as lysophospholipids and free iron, phosphatidylserine exposure and shedding MPs [59]. PubMed:28458720

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Veins
MeSH
beta-Thalassemia
Text Location
Review

a(HM:cytolysin) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Some pathogens are capable of causing hemolysis by cytolytic toxins. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

a(MESH:"Blood Substitutes") increases path(MESH:Hemolysis) View Subject | View Object

Multiple haemolytic disorders and therapeutic interventions produce substantial intravascular haemolysis. Examples include PNH, SCD, thalassaemias, glucose-6-phosphate dehydrogenase (G6PD) deficiency, hereditary spherocytosis and stomatocytosis, pyruvate kinase deficiency, autoimmune haemolytic anaemia, microangiopathies, acute haemolytic transfusion reactions, mechanical circulatory support [e.g., left ventricular assist device (LVAD)/extracorporeal membrane oxygenation (ECMO)], RBC transfusions and infusions of RBC substitutes. These disorders, therapies and procedures are also associated with an increased risk of thrombosis. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Plasma
MeSH
Urine
Text Location
Review

a(MESH:"Blood Transfusion") increases path(MESH:Hemolysis) View Subject | View Object

Multiple haemolytic disorders and therapeutic interventions produce substantial intravascular haemolysis. Examples include PNH, SCD, thalassaemias, glucose-6-phosphate dehydrogenase (G6PD) deficiency, hereditary spherocytosis and stomatocytosis, pyruvate kinase deficiency, autoimmune haemolytic anaemia, microangiopathies, acute haemolytic transfusion reactions, mechanical circulatory support [e.g., left ventricular assist device (LVAD)/extracorporeal membrane oxygenation (ECMO)], RBC transfusions and infusions of RBC substitutes. These disorders, therapies and procedures are also associated with an increased risk of thrombosis. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Plasma
MeSH
Urine
Text Location
Review

a(MESH:"Blood Transfusion") increases path(MESH:Hemolysis) View Subject | View Object

Biochemical and biomechanical changes occur in the RBCs during the storage process, ultimately leading to increased haemolysis upon transfusion (Cohen & Matot, 2013). PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

a(MESH:"Blood Transfusion") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

The plasma hemoglobin levels at two and four hours after SRBC-transfusion were greater than the cell-free hemoglobin levels in the supernatant of the SRBCs before transfusion (Figure 1C, Supplemental Table I), providing evidence that hemolysis occurs in vivo during and after transfusion of SRBCs. PubMed:27515135

Appears in Networks:
Annotations
MeSH
Hemorrhage
Text Location
Results

a(MESH:"Complement C3a") increases path(MESH:Hemolysis) View Subject | View Object

However, also the anaphylatoxins C3a and C5a may lead to cellular and organ disturbances [75]. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

a(MESH:"Complement C5a") increases path(MESH:Hemolysis) View Subject | View Object

However, also the anaphylatoxins C3a and C5a may lead to cellular and organ disturbances [75]. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

a(MESH:"Complement Membrane Attack Complex") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Erythrocyte lysis after ICH can be mediated by the complement activation and formation of the membrane attack complex (MAC), which contains complement C5b, C6, C7, C8 and C9 proteins (C5b– 9). PubMed:27125525

Appears in Networks:
Annotations
Text Location
Introduction

a(MESH:"Complement Membrane Attack Complex") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Activation of the complement system and the formation of MAC resulted in an increased membrane permeability and erythrocyte lysis. PubMed:27125525

Appears in Networks:
Annotations
MeSH
Cerebral Hemorrhage
Text Location
Results

a(MESH:"Complement Membrane Attack Complex") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Following complement cascade activation, MAC on the cell membrane forms a pore resulting in membrane permeability changes17 finally leading to RBC morphological alterations and erythrocyte lysis. PubMed:27125525

Appears in Networks:
Annotations
MeSH
Cerebral Hemorrhage
Text Location
Discussion

a(MESH:"Complement Membrane Attack Complex") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Increased MAC deposition may lead to cell lysis and hemolysis, as is usually seen in RBCs but to a lesser extent in neutrophils and platelets (please see below). PubMed:29929138

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
Cell Ontology (CL)
neutrophil
Cell Ontology (CL)
platelet
MeSH
Hemoglobinuria, Paroxysmal
Text Location
Results

a(MESH:"Complement Membrane Attack Complex") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Following MAC deposition on RBCs, intravascular hemolysis that leads to increasing levels of free hemoglobin was seen. PubMed:29929138

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
Cell Ontology (CL)
neutrophil
Cell Ontology (CL)
platelet
MeSH
Hemoglobinuria, Paroxysmal
Text Location
Results

a(MESH:"Complement Membrane Attack Complex") increases path(MESH:Hemolysis) View Subject | View Object

Ultimately, activation of the complement cascade results in formation of the terminal complement complex C5b-9, the so-called membrane attack complex, and consequently a pore formation resulting in osmotic lysis of the target [71]. In the case of red blood cells, hemolysis will result. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Hemolysis
Text Location
Review

a(MESH:"Extracellular Traps") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Furthermore, haem released during SCD-induced haemolysis triggers the release of neutrophil extracellular traps (NETs) via a ROS-dependent mechanism (Chen et al, 2014). PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

act(a(MESH:Plasmodium)) increases path(MESH:Hemolysis) View Subject | View Object

Plasmodium-mediated lysis of a single infected erythrocyte in vivo was shown to result in the lysis of 8–10 uninfected cells [78,79]. PubMed:26875449

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Anemia, Sickle Cell
Text Location
Review

bp(GO:"complement activation") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Erythrocyte lysis after ICH can be mediated by the complement activation and formation of the membrane attack complex (MAC), which contains complement C5b, C6, C7, C8 and C9 proteins (C5b– 9). PubMed:27125525

Appears in Networks:
Annotations
Text Location
Introduction

bp(GO:"complement activation") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

It is crucial, hence, to further investigate the mechanisms of sepsis-induced hemolysis with the aim of deriving possible therapeutic principles. Herein, we collected the most important previously known triggers of hemolysis during sepsis, which are (1) transfusion reactions and complement activation, (2) disseminated intravascular coagulation, (3) capillary stopped-flow, (4) restriction of glucose to red blood cells, (5) changes in red blood cell membrane properties, (6) hemolytic pathogens, and (7) red blood cell apoptosis. PubMed:29956069

Appears in Networks:
Annotations
Text Location
Review

bp(GO:"complement activation") increases path(MESH:Hemolysis) View Subject | View Object

Thus, the complement system may be causally involved in the onset of hemolysis during sepsis [74] by directly damaging the red blood cells upon activation as a result of detecting pathogen structures [73]. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

bp(GO:vasoconstriction) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Thus, haemolysis results in NO scavenging, systemic vasoconstriction and increased blood stasis, thereby affecting one of the principle components of Virchow’s Triad. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

bp(HM:"Rh incompatibility") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Extravascular hemolysis, however, results from Rh incompatibility of red blood cells [72] and is complement independent [71]. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

bp(MESH:"Blood Group Incompatibility") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Most hemolytic transfusion reactions^ can be attributed to ABO antibodies (ABO incompatibility of red blood cells) leading to intravascular hemolysis [69, 70] as a consequence of robust complement activation [71]. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
hepatocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

bp(MESH:"Blood Coagulation") increases path(MESH:Hemolysis) View Subject | View Object

Similar to HUS, during sepsis an activation not just of the complement system but also of the coagulation system has been described (essentially in consequence of the so-called pro-coagulant shift of the endothelial cells), which offers us the next possible cause of hemolysis during sepsis: destruction of the red blood cells in the fibrin mesh. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

bp(MESH:"Blood Transfusion") increases path(MESH:Hemolysis) View Subject | View Object

Any increase in hemolysis after transfusion of stored RBCs can be attributed to lysis of RBCs during storage or after transfusion (Figure 1B). PubMed:27308950

Appears in Networks:
Annotations
MeSH
Plasma
Text Location
Discussion

bp(MESH:"Erythrocyte Count") negativeCorrelation path(MESH:Hemolysis) View Subject | View Object

The essential feature of any haemolytic disorder is shortened red blood cell (RBC) lifespan. PubMed:25307023

Appears in Networks:
Annotations
Text Location
Review

p(HGNC:HBB) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Hemolysis increases the concentration of Hb which, under oxidative stress, releases free heme. PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Malaria
Text Location
Review

bp(MESH:"Glucose-Galactose Malabsorption") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

It is crucial, hence, to further investigate the mechanisms of sepsis-induced hemolysis with the aim of deriving possible therapeutic principles. Herein, we collected the most important previously known triggers of hemolysis during sepsis, which are (1) transfusion reactions and complement activation, (2) disseminated intravascular coagulation, (3) capillary stopped-flow, (4) restriction of glucose to red blood cells, (5) changes in red blood cell membrane properties, (6) hemolytic pathogens, and (7) red blood cell apoptosis. PubMed:29956069

Appears in Networks:
Annotations
Text Location
Review

bp(MESH:Hemostasis) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Thus, haemolysis results in NO scavenging, systemic vasoconstriction and increased blood stasis, thereby affecting one of the principle components of Virchow’s Triad. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

p(HGNC:HBB) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Haemoglobin and haem levels increase in plasma and urine when haptoglobin and haemopexin scavenging mechanisms are saturated during acute or chronic haemolysis. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Plasma
MeSH
Urine
Text Location
Review

p(HGNC:HBB) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Moreover they have demonstrated that released Hb plays an important role in exacerbating RBC hemolysis, establishing a damaging hemolysis/ oxidative cycle that drives further red cell damage, vascular injury, and thrombosis. PubMed:19276082

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Aorta
Text Location
Discussion

p(HGNC:HBB) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Hemolysis and the transfusion of banked blood or Hb-based therapeutics can result in varying quantities of circulating acellular Hb which can induce life threatening radical generating reactions in patients with a compromised vascular system [60]. PubMed:24486321

Appears in Networks:
Annotations
Text Location
Discussion

p(HGNC:HBB) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Subsequent RBC lysis leads to release of acellular Hb, which, in turn, damages the alveolar epithelial cells. PubMed:26974230

Appears in Networks:
Annotations
MeSH
Alveolar Epithelial Cells
Text Location
Introduction

p(HGNC:HBB) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

The plasma hemoglobin levels at two and four hours after SRBC-transfusion were greater than the cell-free hemoglobin levels in the supernatant of the SRBCs before transfusion (Figure 1C, Supplemental Table I), providing evidence that hemolysis occurs in vivo during and after transfusion of SRBCs. PubMed:27515135

Appears in Networks:
Annotations
MeSH
Hemorrhage
Text Location
Results

p(HGNC:HBB) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Red blood cell hemolysis in sickle cell disease (SCD) releases free hemoglobin. PubMed:28088643

Appears in Networks:
Annotations
MeSH
Erythrocytes
MeSH
Anemia, Sickle Cell
Text Location
Abstract

p(HGNC:HBB) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

During hemolysis, hemoglobin and heme released from red blood cells promote oxidative stress, inflammation and thrombosis. PubMed:29694434

Appears in Networks:
Annotations
Text Location
Introduction

p(HGNC:HBB) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Following MAC deposition on RBCs, intravascular hemolysis that leads to increasing levels of free hemoglobin was seen. PubMed:29929138

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
Cell Ontology (CL)
neutrophil
Cell Ontology (CL)
platelet
MeSH
Hemoglobinuria, Paroxysmal
Text Location
Results

p(HGNC:HBB) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

In infectious diseases, such as malaria and sepsis, high amounts of cell-free hemoglobin and heme were found [8], suggesting that hemolysis during sepsis and systemic inflammation is of pathophysiological relevance. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
hepatocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

p(HGNC:HBB) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Finally, a bi-directional crosstalk between hemolysis and coagulation was postulated with induction of tissue factor by cell-free hemoglobin as potentially central mechanism for hemolysis to trigger coagulation [87]. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Disseminated Intravascular Coagulation
Text Location
Review

p(HGNC:HBB) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

In addition to inflammation, cell-free hemoglobin (Hb) released via hemolysis is a potent inducer of oxidative stress. PubMed:30505280

Appears in Networks:
Annotations
MeSH
Knee
MeSH
Osteoarthritis, Knee
Text Location
Introduction

p(HGNC:HPX) negativeCorrelation path(MESH:Hemolysis) View Subject | View Object

Plasma haptoglobin and hemopexin levels are often depleted in SCD patients and mice due to chronic intravascular hemolysis [21±24]. PubMed:29694434

Appears in Networks:
Annotations
MeSH
Blood Platelets
MeSH
Anemia, Sickle Cell
Text Location
Introduction

p(HGNC:HPX) negativeCorrelation path(MESH:Hemolysis) View Subject | View Object

In cases of extensive and chronic hemolysis, levels of haptoglobin and hemopexin in plasma decrease markedly [20,21]. PubMed:26875449

Appears in Networks:
Annotations
Text Location
Review

p(HGNC:HP) negativeCorrelation path(MESH:Hemolysis) View Subject | View Object

However, in patients with hemolysis Hp depletes early in the course of the disease while levels of Hx remain within the physiologic range for prolonged periods of sustained hemolytic disease [12]. PubMed:26475040

Appears in Networks:
Annotations
MeSH
Anemia, Sickle Cell
Text Location
Abstract

p(HGNC:HP) negativeCorrelation path(MESH:Hemolysis) View Subject | View Object

In cases of extensive and chronic hemolysis, levels of haptoglobin and hemopexin in plasma decrease markedly [20,21]. PubMed:26875449

Appears in Networks:
Annotations
Text Location
Review

p(HGNC:HP) negativeCorrelation path(MESH:Hemolysis) View Subject | View Object

Plasma haptoglobin and hemopexin levels are often depleted in SCD patients and mice due to chronic intravascular hemolysis [21±24]. PubMed:29694434

Appears in Networks:
Annotations
MeSH
Blood Platelets
MeSH
Anemia, Sickle Cell
Text Location
Introduction

p(MGI:Prdx2) negativeCorrelation path(MESH:Hemolysis) View Subject | View Object

Finally, slower Prx-2 reduction correlated with increased H2O2 (10 lM)-induced hemolysis of day 35 RBC compared with day 7 RBC (Fig. 1D). PubMed:25264713

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
Text Location
Results

p(HGNC:ARG1) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Table 3 shows a significant increase in the median value for the plasma biomarker of hemolysis, arginase-1 in patients with PE+TR+ by pairwise comparison using the Kruskal-Wallis test. PubMed:26337933

Appears in Networks:
Annotations
MeSH
Pulmonary Embolism
Text Location
Results

p(HGNC:CD55) decreases path(MESH:Hemolysis) View Subject | View Object

This scenario may resemble that of paroxysmal nocturnal hemoglobinuria patients, who can be treated with complement C5- blocking antibody eculizumab [80]; in this example, extravascular hemolysis has been shown to occur in a small number of these patients despite treatment. It has been suggested that this is due to erythrophagocytosis of red blood cells deficient in the C3d-opsonized complement regulators – CD55 and CD59 [81,82]. PubMed:26875449

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Malaria
Text Location
Review

p(HGNC:CD59) decreases path(MESH:Hemolysis) View Subject | View Object

This scenario may resemble that of paroxysmal nocturnal hemoglobinuria patients, who can be treated with complement C5- blocking antibody eculizumab [80]; in this example, extravascular hemolysis has been shown to occur in a small number of these patients despite treatment. It has been suggested that this is due to erythrophagocytosis of red blood cells deficient in the C3d-opsonized complement regulators – CD55 and CD59 [81,82]. PubMed:26875449

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Malaria
Text Location
Review

p(HGNC:CD59) negativeCorrelation path(MESH:Hemolysis) View Subject | View Object

PIGA encodes a GPI biosynthesis protein, phosphatidylinositol N-acetylglucosaminyltransferase subunit A [5, 6], and erythrocytes deficient in GPI-anchored membrane proteins, including CD59, undergo complement-mediated hemolysis. PubMed:29929138

Appears in Networks:
Annotations
MeSH
Hemoglobinuria, Paroxysmal
Text Location
Introduction

p(HGNC:CD59, var("p.Cys89Tyr")) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

The Cys89Tyr mutation in CD59 was initially described with manifestation in infancy by chronic hemolysis and relapsing peripheral demyelinating disease resembling recurrent Guillain- Barre syndrome (GBS) or chronic inflammatory demyelinating polyneuropathy (CIDP). PubMed:29929138

Appears in Networks:
Annotations
MeSH
Hemoglobinuria, Paroxysmal
Text Location
Introduction

p(HGNC:HAMP) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Our results show that hamp1 levels are significantly elevated in the presence of PHZ but is equivalent in both, WT and DKO fish (S6 Fig). PubMed:30248094

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Kidney
Text Location
Results

p(HGNC:SLC48A1) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

We show that the zebrafish kidney is the primary organ for heme-iron recycling during EP and that zebrafish Hrg1a and Hrg1b are heme transporters that are expressed and upregulated in kidney macrophages after PHZ-induced hemolysis. PubMed:30248094

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Kidney
Text Location
Results

p(MGI:Hrg) decreases path(MESH:Hemolysis) View Subject | View Object

Hemin-induced hemolysis was also inhibited by HRG and HRGderived peptide (amino acid sequence in the Histidine-rich domain of HRG: HHPHGHHPHG) (Fig. 6A and B). PubMed:29544683

Appears in Networks:
Annotations
MeSH
Erythrocyte Membrane
MeSH
Sepsis
Text Location
Results

p(PFAM:Leukocidin) increases path(MESH:Hemolysis) View Subject | View Object

The same applies to hemolysin. For one thing, the pore-forming toxin hemolysin is one the pathogens’ tools of causing hemolysis or releasing hemoglobin and poorly available iron [139]; then again it trigger eryptosis, one mechanism of protecting against hemolysis [142]. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

path(HM:"endothelial lesions") increases path(MESH:Hemolysis) View Subject | View Object

From hemolytic uremic syndrome (HUS), we know that damage to the endothelium (endothelial lesions) might be the primary cause of hemolysis. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Atypical Hemolytic Uremic Syndrome
Text Location
Review

path(HM:"endothelial lesions") increases path(MESH:Hemolysis) View Subject | View Object

During HUS, endothelial lesions cause a complement dependent activation of immune response and local thrombus formation—attachment of fibrin and platelets to the endothelial lesions and consequently disseminated intravascular coagulation (DIC)—and further mechanical destruction of the red blood cells in the fibrin mesh resulting in hemolysis [82]. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Atypical Hemolytic Uremic Syndrome
Text Location
Review

path(HM:"renal stasis") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

There are various studies that show a relationship between microvascular stasis and intravascular hemolysis. Already in 1940, Mumme described that renal stasis causes hemolysis [108]. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Disseminated Intravascular Coagulation
Text Location
Review

path(HP:"Hemolytic-uremic syndrome") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Although haemolysis and thrombosis are hallmarks of the thrombo microangiopathies, such as disseminated intravascular coagulation (DIC) and thrombotic thrombocytopenic purpura/haemolytic uraemic syndrome (TTP/HUS), it is difficult to isolate the causative role of haemolysis in the pathophysiology of thrombosis in these complex disorders. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

path(HP:"Paroxysmal nocturnal hemoglobinuria") increases path(MESH:Hemolysis) View Subject | View Object

Multiple haemolytic disorders and therapeutic interventions produce substantial intravascular haemolysis. Examples include PNH, SCD, thalassaemias, glucose-6-phosphate dehydrogenase (G6PD) deficiency, hereditary spherocytosis and stomatocytosis, pyruvate kinase deficiency, autoimmune haemolytic anaemia, microangiopathies, acute haemolytic transfusion reactions, mechanical circulatory support [e.g., left ventricular assist device (LVAD)/extracorporeal membrane oxygenation (ECMO)], RBC transfusions and infusions of RBC substitutes. These disorders, therapies and procedures are also associated with an increased risk of thrombosis. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Plasma
MeSH
Urine
Text Location
Review

path(HP:"Paroxysmal nocturnal hemoglobinuria") increases path(MESH:Hemolysis) View Subject | View Object

In PNH, uncontrolled complement activity leads to systemic complications, principally through intravascular haemolysis and platelet activation. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Plasma
MeSH
Urine
Text Location
Review

path(HP:"Paroxysmal nocturnal hemoglobinuria") association path(MESH:Hemolysis) View Subject | View Object

Inhibition of the terminal complement cascade by eculizumab (inhibits the cleavage of C5 into C5a und C5b and thus the formation of the membrane attack complex 8, MAC C5b-C9) for the treatment of hemolytic paroxymal nocturnal hemoglobinuria (PNH) significantly prevented PNH-related symptoms in patients including abnormal thrombophilia, red blood cell destruction, and the extent of hemolysis [76]. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

path(HP:"autoimmune hemolytic anemia") increases path(MESH:Hemolysis) View Subject | View Object

Multiple haemolytic disorders and therapeutic interventions produce substantial intravascular haemolysis. Examples include PNH, SCD, thalassaemias, glucose-6-phosphate dehydrogenase (G6PD) deficiency, hereditary spherocytosis and stomatocytosis, pyruvate kinase deficiency, autoimmune haemolytic anaemia, microangiopathies, acute haemolytic transfusion reactions, mechanical circulatory support [e.g., left ventricular assist device (LVAD)/extracorporeal membrane oxygenation (ECMO)], RBC transfusions and infusions of RBC substitutes. These disorders, therapies and procedures are also associated with an increased risk of thrombosis. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Plasma
MeSH
Urine
Text Location
Review

path(HP:Stomatocytosis) increases path(MESH:Hemolysis) View Subject | View Object

Multiple haemolytic disorders and therapeutic interventions produce substantial intravascular haemolysis. Examples include PNH, SCD, thalassaemias, glucose-6-phosphate dehydrogenase (G6PD) deficiency, hereditary spherocytosis and stomatocytosis, pyruvate kinase deficiency, autoimmune haemolytic anaemia, microangiopathies, acute haemolytic transfusion reactions, mechanical circulatory support [e.g., left ventricular assist device (LVAD)/extracorporeal membrane oxygenation (ECMO)], RBC transfusions and infusions of RBC substitutes. These disorders, therapies and procedures are also associated with an increased risk of thrombosis. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Plasma
MeSH
Urine
Text Location
Review

path(MESH:"Acute Kidney Injury") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Therefore, acute kidney injury (AKI) remains an important complication of acute and severe intravascular hemolysis. PubMed:26794659

Appears in Networks:
Annotations
MeSH
Liver
Text Location
Introduction

path(MESH:"Anemia, Sickle Cell") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

SCD and β-thalassemia are genetic diseases associated to erythrocytes that are prone to lysis due to defective Hb production (Heinle and Read, 1948; Pauling et al., 1949; Ingram, 1957; discussed later). PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Rhabdomyolysis
Text Location
Review

path(MESH:"Anemia, Sickle Cell") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Hemolysis can happen due to ischemia/reperfusion, SCD or β-thalassemia. PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Malaria
Text Location
Review

path(MESH:"Anemia, Sickle Cell") increases path(MESH:Hemolysis) View Subject | View Object

Multiple haemolytic disorders and therapeutic interventions produce substantial intravascular haemolysis. Examples include PNH, SCD, thalassaemias, glucose-6-phosphate dehydrogenase (G6PD) deficiency, hereditary spherocytosis and stomatocytosis, pyruvate kinase deficiency, autoimmune haemolytic anaemia, microangiopathies, acute haemolytic transfusion reactions, mechanical circulatory support [e.g., left ventricular assist device (LVAD)/extracorporeal membrane oxygenation (ECMO)], RBC transfusions and infusions of RBC substitutes. These disorders, therapies and procedures are also associated with an increased risk of thrombosis. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Plasma
MeSH
Urine
Text Location
Review

path(MESH:"Anemia, Sickle Cell") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

SCD is a haemolytic disorder caused by a HBB (b-globin gene) mutation leading to polymerization of haemoglobin S, sickling, and haemolysis. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Plasma
MeSH
Urine
MeSH
Hemoglobinuria, Paroxysmal
Text Location
Review

path(MESH:"Anemia, Sickle Cell") increases path(MESH:Hemolysis) View Subject | View Object

Systemic hemolysis occurs during certain genetic and acquired anemia, such as in sickle cell disease and malaria. PubMed:26475040

Appears in Networks:
Annotations
MeSH
Anemia, Sickle Cell
Text Location
Abstract

path(MESH:"Disseminated Intravascular Coagulation") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Although haemolysis and thrombosis are hallmarks of the thrombo microangiopathies, such as disseminated intravascular coagulation (DIC) and thrombotic thrombocytopenic purpura/haemolytic uraemic syndrome (TTP/HUS), it is difficult to isolate the causative role of haemolysis in the pathophysiology of thrombosis in these complex disorders. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

path(MESH:"Disseminated Intravascular Coagulation") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

It is crucial, hence, to further investigate the mechanisms of sepsis-induced hemolysis with the aim of deriving possible therapeutic principles. Herein, we collected the most important previously known triggers of hemolysis during sepsis, which are (1) transfusion reactions and complement activation, (2) disseminated intravascular coagulation, (3) capillary stopped-flow, (4) restriction of glucose to red blood cells, (5) changes in red blood cell membrane properties, (6) hemolytic pathogens, and (7) red blood cell apoptosis. PubMed:29956069

Appears in Networks:
Annotations
Text Location
Review

path(MESH:"Pulmonary Embolism") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

We hypothesize acute moderate to severe PE causes turbulent flow across the tricuspid and pulmonic valves and in the pulmonary tree, causing rupture of a small percentage of red cells in or immediately proximal to or within the pulmonary vascular tree. PubMed:26337933

Appears in Networks:
Annotations
Cell Ontology (CL)
leukocyte
MeSH
Pulmonary Embolism
Text Location
Discussion

path(MESH:"Pyruvate Kinase Deficiency of Red Cells") increases path(MESH:Hemolysis) View Subject | View Object

Multiple haemolytic disorders and therapeutic interventions produce substantial intravascular haemolysis. Examples include PNH, SCD, thalassaemias, glucose-6-phosphate dehydrogenase (G6PD) deficiency, hereditary spherocytosis and stomatocytosis, pyruvate kinase deficiency, autoimmune haemolytic anaemia, microangiopathies, acute haemolytic transfusion reactions, mechanical circulatory support [e.g., left ventricular assist device (LVAD)/extracorporeal membrane oxygenation (ECMO)], RBC transfusions and infusions of RBC substitutes. These disorders, therapies and procedures are also associated with an increased risk of thrombosis. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Plasma
MeSH
Urine
Text Location
Review

path(MESH:"Shock, Traumatic") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Thus, hemolysis can act as a kind of amplifier of the complex response to an infection or injury [8, 15] and worsen the outcome from animals and patients with systemic inflammation, sepsis, or trauma [1–4, 10]. PubMed:29956069

Appears in Networks:
Annotations
Text Location
Review

path(MESH:"Spherocytosis, Hereditary") increases path(MESH:Hemolysis) View Subject | View Object

Multiple haemolytic disorders and therapeutic interventions produce substantial intravascular haemolysis. Examples include PNH, SCD, thalassaemias, glucose-6-phosphate dehydrogenase (G6PD) deficiency, hereditary spherocytosis and stomatocytosis, pyruvate kinase deficiency, autoimmune haemolytic anaemia, microangiopathies, acute haemolytic transfusion reactions, mechanical circulatory support [e.g., left ventricular assist device (LVAD)/extracorporeal membrane oxygenation (ECMO)], RBC transfusions and infusions of RBC substitutes. These disorders, therapies and procedures are also associated with an increased risk of thrombosis. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Plasma
MeSH
Urine
Text Location
Review

path(MESH:"Thrombotic Microangiopathies") increases path(MESH:Hemolysis) View Subject | View Object

Multiple haemolytic disorders and therapeutic interventions produce substantial intravascular haemolysis. Examples include PNH, SCD, thalassaemias, glucose-6-phosphate dehydrogenase (G6PD) deficiency, hereditary spherocytosis and stomatocytosis, pyruvate kinase deficiency, autoimmune haemolytic anaemia, microangiopathies, acute haemolytic transfusion reactions, mechanical circulatory support [e.g., left ventricular assist device (LVAD)/extracorporeal membrane oxygenation (ECMO)], RBC transfusions and infusions of RBC substitutes. These disorders, therapies and procedures are also associated with an increased risk of thrombosis. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Plasma
MeSH
Urine
Text Location
Review

path(MESH:"Thrombotic Microangiopathies") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Although haemolysis and thrombosis are hallmarks of the thrombo microangiopathies, such as disseminated intravascular coagulation (DIC) and thrombotic thrombocytopenic purpura/haemolytic uraemic syndrome (TTP/HUS), it is difficult to isolate the causative role of haemolysis in the pathophysiology of thrombosis in these complex disorders. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

path(MESH:"Transfusion Reaction") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

It is crucial, hence, to further investigate the mechanisms of sepsis-induced hemolysis with the aim of deriving possible therapeutic principles. Herein, we collected the most important previously known triggers of hemolysis during sepsis, which are (1) transfusion reactions and complement activation, (2) disseminated intravascular coagulation, (3) capillary stopped-flow, (4) restriction of glucose to red blood cells, (5) changes in red blood cell membrane properties, (6) hemolytic pathogens, and (7) red blood cell apoptosis. PubMed:29956069

Appears in Networks:
Annotations
Text Location
Review

path(MESH:"Vascular Diseases") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Furthermore, experiments of nature that lead to increased levels of chronic hemolysis, such as sickle cell anemia and paroxysmal nocturnal hemoglobinuria, provide evidence that low levels of hemolysis may be harmful, and contribute to inflammation, thrombosis, vasculopathy, and impaired host defenses against infection.1,11 PubMed:29603246

Appears in Networks:
Annotations
MeSH
Anemia, Sickle Cell
Text Location
Introduction

path(MESH:"Vascular System Injuries") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Moreover they have demonstrated that released Hb plays an important role in exacerbating RBC hemolysis, establishing a damaging hemolysis/ oxidative cycle that drives further red cell damage, vascular injury, and thrombosis. PubMed:19276082

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Aorta
Text Location
Discussion

path(MESH:"beta-Thalassemia") positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

SCD and β-thalassemia are genetic diseases associated to erythrocytes that are prone to lysis due to defective Hb production (Heinle and Read, 1948; Pauling et al., 1949; Ingram, 1957; discussed later). PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Rhabdomyolysis
Text Location
Review

path(MESH:Inflammation) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Furthermore, experiments of nature that lead to increased levels of chronic hemolysis, such as sickle cell anemia and paroxysmal nocturnal hemoglobinuria, provide evidence that low levels of hemolysis may be harmful, and contribute to inflammation, thrombosis, vasculopathy, and impaired host defenses against infection.1,11 PubMed:29603246

Appears in Networks:
Annotations
MeSH
Anemia, Sickle Cell
Text Location
Introduction

path(MESH:Inflammation) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Thus, hemolysis can act as a kind of amplifier of the complex response to an infection or injury [8, 15] and worsen the outcome from animals and patients with systemic inflammation, sepsis, or trauma [1–4, 10]. PubMed:29956069

Appears in Networks:
Annotations
Text Location
Review

path(MESH:Ischemia) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Hemolysis can happen due to ischemia/reperfusion, SCD or β-thalassemia. PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Malaria
Text Location
Review

path(MESH:Malaria) increases path(MESH:Hemolysis) View Subject | View Object

Systemic hemolysis occurs during certain genetic and acquired anemia, such as in sickle cell disease and malaria. PubMed:26475040

Appears in Networks:
Annotations
MeSH
Anemia, Sickle Cell
Text Location
Abstract

path(MESH:Sepsis) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Both clinical [1–4] and experimental [5–8] studies have shown that sepsis and systemic inflammation lead to a massive release of hemoglobin from red blood cells (hemolysis) being accompanied with an increased risk of death [1–4, 8, 9]. PubMed:29956069

Appears in Networks:
Annotations
Text Location
Review

path(MESH:Sepsis) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Thus, hemolysis can act as a kind of amplifier of the complex response to an infection or injury [8, 15] and worsen the outcome from animals and patients with systemic inflammation, sepsis, or trauma [1–4, 10]. PubMed:29956069

Appears in Networks:
Annotations
Text Location
Review

path(MESH:Thalassemia) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Hemolysis can happen due to ischemia/reperfusion, SCD or β-thalassemia. PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Malaria
Text Location
Review

path(MESH:Thalassemia) increases path(MESH:Hemolysis) View Subject | View Object

Multiple haemolytic disorders and therapeutic interventions produce substantial intravascular haemolysis. Examples include PNH, SCD, thalassaemias, glucose-6-phosphate dehydrogenase (G6PD) deficiency, hereditary spherocytosis and stomatocytosis, pyruvate kinase deficiency, autoimmune haemolytic anaemia, microangiopathies, acute haemolytic transfusion reactions, mechanical circulatory support [e.g., left ventricular assist device (LVAD)/extracorporeal membrane oxygenation (ECMO)], RBC transfusions and infusions of RBC substitutes. These disorders, therapies and procedures are also associated with an increased risk of thrombosis. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Plasma
MeSH
Urine
Text Location
Review

path(MESH:Thrombophilia) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Intravascular hemolysis is one thrombophilic mechanisms in PNH (reviewed by Hill et al. [14]). PubMed:29929138

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
Cell Ontology (CL)
neutrophil
Cell Ontology (CL)
platelet
MeSH
Hemoglobinuria, Paroxysmal
Text Location
Discussion

path(MESH:Thrombosis) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Moreover they have demonstrated that released Hb plays an important role in exacerbating RBC hemolysis, establishing a damaging hemolysis/ oxidative cycle that drives further red cell damage, vascular injury, and thrombosis. PubMed:19276082

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Aorta
Text Location
Discussion

path(MESH:Thrombosis) association path(MESH:Hemolysis) View Subject | View Object

Haemolysis, which is observed in multiple diseases, can affect all three components of Virchow’s triad; thus, it is not surprising that there is a link between haemolytic disorders and thrombosis. PubMed:25307023

Appears in Networks:
Annotations
Text Location
Review

path(MESH:Thrombosis) positiveCorrelation path(MESH:Hemolysis) View Subject | View Object

Furthermore, experiments of nature that lead to increased levels of chronic hemolysis, such as sickle cell anemia and paroxysmal nocturnal hemoglobinuria, provide evidence that low levels of hemolysis may be harmful, and contribute to inflammation, thrombosis, vasculopathy, and impaired host defenses against infection.1,11 PubMed:29603246

Appears in Networks:
Annotations
MeSH
Anemia, Sickle Cell
Text Location
Introduction

Out-Edges 87

path(MESH:Hemolysis) positiveCorrelation path(MESH:Thalassemia) View Subject | View Object

Hemolysis can happen due to ischemia/reperfusion, SCD or β-thalassemia. PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Malaria
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation path(MESH:Sepsis) View Subject | View Object

Thus, hemolysis can act as a kind of amplifier of the complex response to an infection or injury [8, 15] and worsen the outcome from animals and patients with systemic inflammation, sepsis, or trauma [1–4, 10]. PubMed:29956069

Appears in Networks:
Annotations
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation a(CHEBI:heme) View Subject | View Object

Haemoglobin and haem levels increase in plasma and urine when haptoglobin and haemopexin scavenging mechanisms are saturated during acute or chronic haemolysis. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Plasma
MeSH
Urine
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation a(CHEBI:"iron trichloride") View Subject | View Object

Analysis of the time course of hemolysis in whole blood revealed a rapid linear increase in Hb levels, peaking 10 min after FeCl3 addition (Fig. 2B), a time course consistent with the rapid hemolysis and vascular injury observed in the ex vivo aortic thrombosis model. PubMed:19276082

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Aorta
Text Location
Introduction

path(MESH:Hemolysis) positiveCorrelation p(HGNC:HBB) View Subject | View Object

Moreover they have demonstrated that released Hb plays an important role in exacerbating RBC hemolysis, establishing a damaging hemolysis/ oxidative cycle that drives further red cell damage, vascular injury, and thrombosis. PubMed:19276082

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Aorta
Text Location
Discussion

path(MESH:Hemolysis) positiveCorrelation p(HGNC:HBB) View Subject | View Object

Hemolysis and the transfusion of banked blood or Hb-based therapeutics can result in varying quantities of circulating acellular Hb which can induce life threatening radical generating reactions in patients with a compromised vascular system [60]. PubMed:24486321

Appears in Networks:
Annotations
Text Location
Discussion

path(MESH:Hemolysis) positiveCorrelation p(HGNC:HBB) View Subject | View Object

Hemolysis increases the concentration of Hb which, under oxidative stress, releases free heme. PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Malaria
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation p(HGNC:HBB) View Subject | View Object

Haemoglobin and haem levels increase in plasma and urine when haptoglobin and haemopexin scavenging mechanisms are saturated during acute or chronic haemolysis. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Plasma
MeSH
Urine
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation p(HGNC:HBB) View Subject | View Object

Subsequent RBC lysis leads to release of acellular Hb, which, in turn, damages the alveolar epithelial cells. PubMed:26974230

Appears in Networks:
Annotations
MeSH
Alveolar Epithelial Cells
Text Location
Introduction

path(MESH:Hemolysis) positiveCorrelation p(HGNC:HBB) View Subject | View Object

The plasma hemoglobin levels at two and four hours after SRBC-transfusion were greater than the cell-free hemoglobin levels in the supernatant of the SRBCs before transfusion (Figure 1C, Supplemental Table I), providing evidence that hemolysis occurs in vivo during and after transfusion of SRBCs. PubMed:27515135

Appears in Networks:
Annotations
MeSH
Hemorrhage
Text Location
Results

path(MESH:Hemolysis) positiveCorrelation p(HGNC:HBB) View Subject | View Object

Red blood cell hemolysis in sickle cell disease (SCD) releases free hemoglobin. PubMed:28088643

Appears in Networks:
Annotations
MeSH
Erythrocytes
MeSH
Anemia, Sickle Cell
Text Location
Abstract

path(MESH:Hemolysis) positiveCorrelation p(HGNC:HBB) View Subject | View Object

During hemolysis, hemoglobin and heme released from red blood cells promote oxidative stress, inflammation and thrombosis. PubMed:29694434

Appears in Networks:
Annotations
Text Location
Introduction

path(MESH:Hemolysis) positiveCorrelation p(HGNC:HBB) View Subject | View Object

Following MAC deposition on RBCs, intravascular hemolysis that leads to increasing levels of free hemoglobin was seen. PubMed:29929138

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
Cell Ontology (CL)
neutrophil
Cell Ontology (CL)
platelet
MeSH
Hemoglobinuria, Paroxysmal
Text Location
Results

path(MESH:Hemolysis) increases p(HGNC:HBB) View Subject | View Object

Excessive intravascular hemolysis saturates scavenger mechanisms, resulting in free hemoglobin in plasma that irreversibly reacts with nitric oxide (NO) to form nitrate and methemoglobin. PubMed:29929138

Appears in Networks:
Annotations
Cell Ontology (CL)
platelet
MeSH
Hemoglobinuria, Paroxysmal
Text Location
Discussion

path(MESH:Hemolysis) positiveCorrelation p(HGNC:HBB) View Subject | View Object

In infectious diseases, such as malaria and sepsis, high amounts of cell-free hemoglobin and heme were found [8], suggesting that hemolysis during sepsis and systemic inflammation is of pathophysiological relevance. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
hepatocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation p(HGNC:HBB) View Subject | View Object

Finally, a bi-directional crosstalk between hemolysis and coagulation was postulated with induction of tissue factor by cell-free hemoglobin as potentially central mechanism for hemolysis to trigger coagulation [87]. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Disseminated Intravascular Coagulation
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation p(HGNC:HBB) View Subject | View Object

In addition to inflammation, cell-free hemoglobin (Hb) released via hemolysis is a potent inducer of oxidative stress. PubMed:30505280

Appears in Networks:
Annotations
MeSH
Knee
MeSH
Osteoarthritis, Knee
Text Location
Introduction

path(MESH:Hemolysis) positiveCorrelation path(MESH:"Vascular System Injuries") View Subject | View Object

Moreover they have demonstrated that released Hb plays an important role in exacerbating RBC hemolysis, establishing a damaging hemolysis/ oxidative cycle that drives further red cell damage, vascular injury, and thrombosis. PubMed:19276082

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Aorta
Text Location
Discussion

path(MESH:Hemolysis) positiveCorrelation path(MESH:Thrombosis) View Subject | View Object

Moreover they have demonstrated that released Hb plays an important role in exacerbating RBC hemolysis, establishing a damaging hemolysis/ oxidative cycle that drives further red cell damage, vascular injury, and thrombosis. PubMed:19276082

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Aorta
Text Location
Discussion

path(MESH:Hemolysis) association path(MESH:Thrombosis) View Subject | View Object

Haemolysis, which is observed in multiple diseases, can affect all three components of Virchow’s triad; thus, it is not surprising that there is a link between haemolytic disorders and thrombosis. PubMed:25307023

Appears in Networks:
Annotations
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation path(MESH:Thrombosis) View Subject | View Object

Furthermore, experiments of nature that lead to increased levels of chronic hemolysis, such as sickle cell anemia and paroxysmal nocturnal hemoglobinuria, provide evidence that low levels of hemolysis may be harmful, and contribute to inflammation, thrombosis, vasculopathy, and impaired host defenses against infection.1,11 PubMed:29603246

Appears in Networks:
Annotations
MeSH
Anemia, Sickle Cell
Text Location
Introduction

path(MESH:Hemolysis) positiveCorrelation a(CHEBI:heme) View Subject | View Object

Free heme is generated by intra- and extra-vascular hemolysis or extensive cell damage [14, 15]. PubMed:24464629

Appears in Networks:
Annotations
MeSH
Kidney
Text Location
Introduction

path(MESH:Hemolysis) positiveCorrelation a(CHEBI:heme) View Subject | View Object

Lysis of red blood cells with consequent increases in free heme most likely caused the increase in HO-1 activity responsible for increased COHb concentrations, which is similar to that observed with circulatory devices [6]. PubMed:24553061

Appears in Networks:
Annotations
Text Location
Discussion

path(MESH:Hemolysis) positiveCorrelation a(CHEBI:heme) View Subject | View Object

The above-discussed findings provide strong in vivo evidence that high concentrations of ferric Hb(Fe3+) and free heme can accumulate in the renal cortex during hemolysis. PubMed:26794659

Appears in Networks:
Annotations
Cell Ontology (CL)
epithelial cell
MeSH
Kidney Cortex
Text Location
Discussion

path(MESH:Hemolysis) positiveCorrelation a(CHEBI:heme) View Subject | View Object

During hemolysis, hemoglobin and heme released from red blood cells promote oxidative stress, inflammation and thrombosis. PubMed:29694434

Appears in Networks:
Annotations
Text Location
Introduction

path(MESH:Hemolysis) positiveCorrelation a(CHEBI:heme) View Subject | View Object

In infectious diseases, such as malaria and sepsis, high amounts of cell-free hemoglobin and heme were found [8], suggesting that hemolysis during sepsis and systemic inflammation is of pathophysiological relevance. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
hepatocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation path(MESH:"Anemia, Sickle Cell") View Subject | View Object

SCD and β-thalassemia are genetic diseases associated to erythrocytes that are prone to lysis due to defective Hb production (Heinle and Read, 1948; Pauling et al., 1949; Ingram, 1957; discussed later). PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Rhabdomyolysis
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation path(MESH:"Anemia, Sickle Cell") View Subject | View Object

Hemolysis can happen due to ischemia/reperfusion, SCD or β-thalassemia. PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Malaria
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation path(MESH:"Anemia, Sickle Cell") View Subject | View Object

SCD is a haemolytic disorder caused by a HBB (b-globin gene) mutation leading to polymerization of haemoglobin S, sickling, and haemolysis. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Plasma
MeSH
Urine
MeSH
Hemoglobinuria, Paroxysmal
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation path(MESH:"beta-Thalassemia") View Subject | View Object

SCD and β-thalassemia are genetic diseases associated to erythrocytes that are prone to lysis due to defective Hb production (Heinle and Read, 1948; Pauling et al., 1949; Ingram, 1957; discussed later). PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Rhabdomyolysis
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation path(MESH:Ischemia) View Subject | View Object

Hemolysis can happen due to ischemia/reperfusion, SCD or β-thalassemia. PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Malaria
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation a(CHEBI:"hydrogen peroxide") View Subject | View Object

Finally, slower Prx-2 reduction correlated with increased H2O2 (10 lM)-induced hemolysis of day 35 RBC compared with day 7 RBC (Fig. 1D). PubMed:25264713

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
Text Location
Results

path(MESH:Hemolysis) negativeCorrelation p(MGI:Prdx2) View Subject | View Object

Finally, slower Prx-2 reduction correlated with increased H2O2 (10 lM)-induced hemolysis of day 35 RBC compared with day 7 RBC (Fig. 1D). PubMed:25264713

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
Text Location
Results

path(MESH:Hemolysis) negativeCorrelation bp(MESH:"Erythrocyte Count") View Subject | View Object

The essential feature of any haemolytic disorder is shortened red blood cell (RBC) lifespan. PubMed:25307023

Appears in Networks:
Annotations
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation a(HM:"Glucose-6-phosphate dehydrogenase deficiency") View Subject | View Object

This common X-linked inherited disorder, characterized by severe intravascular and extravascular haemolysis, is classically triggered by fava bean ingestion or pro-oxidant medications. It causes haemolysis in susceptible individuals and an association with thrombosis was described in multiple case reports (Jewett, 1976; Thompson et al, 2013; Albertsen et al, 2014). PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation path(MESH:"Thrombotic Microangiopathies") View Subject | View Object

Although haemolysis and thrombosis are hallmarks of the thrombo microangiopathies, such as disseminated intravascular coagulation (DIC) and thrombotic thrombocytopenic purpura/haemolytic uraemic syndrome (TTP/HUS), it is difficult to isolate the causative role of haemolysis in the pathophysiology of thrombosis in these complex disorders. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation path(MESH:"Disseminated Intravascular Coagulation") View Subject | View Object

Although haemolysis and thrombosis are hallmarks of the thrombo microangiopathies, such as disseminated intravascular coagulation (DIC) and thrombotic thrombocytopenic purpura/haemolytic uraemic syndrome (TTP/HUS), it is difficult to isolate the causative role of haemolysis in the pathophysiology of thrombosis in these complex disorders. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation path(MESH:"Disseminated Intravascular Coagulation") View Subject | View Object

It is crucial, hence, to further investigate the mechanisms of sepsis-induced hemolysis with the aim of deriving possible therapeutic principles. Herein, we collected the most important previously known triggers of hemolysis during sepsis, which are (1) transfusion reactions and complement activation, (2) disseminated intravascular coagulation, (3) capillary stopped-flow, (4) restriction of glucose to red blood cells, (5) changes in red blood cell membrane properties, (6) hemolytic pathogens, and (7) red blood cell apoptosis. PubMed:29956069

Appears in Networks:
Annotations
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation path(HP:"Hemolytic-uremic syndrome") View Subject | View Object

Although haemolysis and thrombosis are hallmarks of the thrombo microangiopathies, such as disseminated intravascular coagulation (DIC) and thrombotic thrombocytopenic purpura/haemolytic uraemic syndrome (TTP/HUS), it is difficult to isolate the causative role of haemolysis in the pathophysiology of thrombosis in these complex disorders. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

path(MESH:Hemolysis) decreases a(CHEBI:"nitric oxide") View Subject | View Object

During intravascular haemolysis, NO availability is severely limited by its reaction with oxyhaemoglobin (i.e., NO scavenging) and by breakdown of the substrate for NO synthesis, L-arginine, by arginase released from RBCs (Schnog et al, 2004). PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation bp(GO:vasoconstriction) View Subject | View Object

Thus, haemolysis results in NO scavenging, systemic vasoconstriction and increased blood stasis, thereby affecting one of the principle components of Virchow’s Triad. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation bp(MESH:Hemostasis) View Subject | View Object

Thus, haemolysis results in NO scavenging, systemic vasoconstriction and increased blood stasis, thereby affecting one of the principle components of Virchow’s Triad. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation a(MESH:"Extracellular Traps") View Subject | View Object

Furthermore, haem released during SCD-induced haemolysis triggers the release of neutrophil extracellular traps (NETs) via a ROS-dependent mechanism (Chen et al, 2014). PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation a(HM:"stored erythrocytes") View Subject | View Object

Storage is known to result in increased hemolysis which in turn results in loss of NO-signaling, oxidative stress and inflammation post-transfusion. PubMed:26202471

Appears in Networks:
Annotations
Text Location
Discussion

path(MESH:Hemolysis) positiveCorrelation p(HGNC:ARG1) View Subject | View Object

Table 3 shows a significant increase in the median value for the plasma biomarker of hemolysis, arginase-1 in patients with PE+TR+ by pairwise comparison using the Kruskal-Wallis test. PubMed:26337933

Appears in Networks:
Annotations
MeSH
Pulmonary Embolism
Text Location
Results

path(MESH:Hemolysis) positiveCorrelation path(MESH:"Pulmonary Embolism") View Subject | View Object

We hypothesize acute moderate to severe PE causes turbulent flow across the tricuspid and pulmonic valves and in the pulmonary tree, causing rupture of a small percentage of red cells in or immediately proximal to or within the pulmonary vascular tree. PubMed:26337933

Appears in Networks:
Annotations
Cell Ontology (CL)
leukocyte
MeSH
Pulmonary Embolism
Text Location
Discussion

path(MESH:Hemolysis) negativeCorrelation p(HGNC:HP) View Subject | View Object

However, in patients with hemolysis Hp depletes early in the course of the disease while levels of Hx remain within the physiologic range for prolonged periods of sustained hemolytic disease [12]. PubMed:26475040

Appears in Networks:
Annotations
MeSH
Anemia, Sickle Cell
Text Location
Abstract

path(MESH:Hemolysis) negativeCorrelation p(HGNC:HP) View Subject | View Object

In cases of extensive and chronic hemolysis, levels of haptoglobin and hemopexin in plasma decrease markedly [20,21]. PubMed:26875449

Appears in Networks:
Annotations
Text Location
Review

path(MESH:Hemolysis) negativeCorrelation p(HGNC:HP) View Subject | View Object

Plasma haptoglobin and hemopexin levels are often depleted in SCD patients and mice due to chronic intravascular hemolysis [21±24]. PubMed:29694434

Appears in Networks:
Annotations
MeSH
Blood Platelets
MeSH
Anemia, Sickle Cell
Text Location
Introduction

path(MESH:Hemolysis) positiveCorrelation path(MESH:"Acute Kidney Injury") View Subject | View Object

Therefore, acute kidney injury (AKI) remains an important complication of acute and severe intravascular hemolysis. PubMed:26794659

Appears in Networks:
Annotations
MeSH
Liver
Text Location
Introduction

path(MESH:Hemolysis) positiveCorrelation a(CHEBI:methemoglobin) View Subject | View Object

The above-discussed findings provide strong in vivo evidence that high concentrations of ferric Hb(Fe3+) and free heme can accumulate in the renal cortex during hemolysis. PubMed:26794659

Appears in Networks:
Annotations
Cell Ontology (CL)
epithelial cell
MeSH
Kidney Cortex
Text Location
Discussion

path(MESH:Hemolysis) negativeCorrelation p(HGNC:HPX) View Subject | View Object

In cases of extensive and chronic hemolysis, levels of haptoglobin and hemopexin in plasma decrease markedly [20,21]. PubMed:26875449

Appears in Networks:
Annotations
Text Location
Review

path(MESH:Hemolysis) negativeCorrelation p(HGNC:HPX) View Subject | View Object

Plasma haptoglobin and hemopexin levels are often depleted in SCD patients and mice due to chronic intravascular hemolysis [21±24]. PubMed:29694434

Appears in Networks:
Annotations
MeSH
Blood Platelets
MeSH
Anemia, Sickle Cell
Text Location
Introduction

path(MESH:Hemolysis) increases a(MESH:"Cell-Derived Microparticles") View Subject | View Object

Interestingly, a recent study demonstrated that, in severe hemolytic disease (sickle cell anemia), at least one third of plasma heme was associated with membrane vesicle structures (microparticles) that were generated from erythrocytes during hemolysis [24]. PubMed:26875449

Appears in Networks:
Annotations
Text Location
Review

path(MESH:Hemolysis) increases a(MESH:"Cell-Derived Microparticles") View Subject | View Object

Third, hemolysis results in a massive release of procoagulant RBC-derived MPs [66]. PubMed:28458720

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Veins
MeSH
beta-Thalassemia
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation bp(GO:"complement activation") View Subject | View Object

Erythrocyte lysis after ICH can be mediated by the complement activation and formation of the membrane attack complex (MAC), which contains complement C5b, C6, C7, C8 and C9 proteins (C5b– 9). PubMed:27125525

Appears in Networks:
Annotations
Text Location
Introduction

path(MESH:Hemolysis) positiveCorrelation bp(GO:"complement activation") View Subject | View Object

Activation of the complement system and the formation of MAC resulted in an increased membrane permeability and erythrocyte lysis. PubMed:27125525

Appears in Networks:
Annotations
MeSH
Cerebral Hemorrhage
Text Location
Results

path(MESH:Hemolysis) positiveCorrelation bp(GO:"complement activation") View Subject | View Object

It is crucial, hence, to further investigate the mechanisms of sepsis-induced hemolysis with the aim of deriving possible therapeutic principles. Herein, we collected the most important previously known triggers of hemolysis during sepsis, which are (1) transfusion reactions and complement activation, (2) disseminated intravascular coagulation, (3) capillary stopped-flow, (4) restriction of glucose to red blood cells, (5) changes in red blood cell membrane properties, (6) hemolytic pathogens, and (7) red blood cell apoptosis. PubMed:29956069

Appears in Networks:
Annotations
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation a(MESH:"Complement Membrane Attack Complex") View Subject | View Object

Erythrocyte lysis after ICH can be mediated by the complement activation and formation of the membrane attack complex (MAC), which contains complement C5b, C6, C7, C8 and C9 proteins (C5b– 9). PubMed:27125525

Appears in Networks:
Annotations
Text Location
Introduction

path(MESH:Hemolysis) positiveCorrelation a(MESH:"Complement Membrane Attack Complex") View Subject | View Object

Activation of the complement system and the formation of MAC resulted in an increased membrane permeability and erythrocyte lysis. PubMed:27125525

Appears in Networks:
Annotations
MeSH
Cerebral Hemorrhage
Text Location
Results

path(MESH:Hemolysis) positiveCorrelation a(MESH:"Complement Membrane Attack Complex") View Subject | View Object

Following complement cascade activation, MAC on the cell membrane forms a pore resulting in membrane permeability changes17 finally leading to RBC morphological alterations and erythrocyte lysis. PubMed:27125525

Appears in Networks:
Annotations
MeSH
Cerebral Hemorrhage
Text Location
Discussion

path(MESH:Hemolysis) positiveCorrelation a(MESH:"Complement Membrane Attack Complex") View Subject | View Object

Increased MAC deposition may lead to cell lysis and hemolysis, as is usually seen in RBCs but to a lesser extent in neutrophils and platelets (please see below). PubMed:29929138

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
Cell Ontology (CL)
neutrophil
Cell Ontology (CL)
platelet
MeSH
Hemoglobinuria, Paroxysmal
Text Location
Results

path(MESH:Hemolysis) positiveCorrelation a(MESH:"Complement Membrane Attack Complex") View Subject | View Object

Following MAC deposition on RBCs, intravascular hemolysis that leads to increasing levels of free hemoglobin was seen. PubMed:29929138

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
Cell Ontology (CL)
neutrophil
Cell Ontology (CL)
platelet
MeSH
Hemoglobinuria, Paroxysmal
Text Location
Results

path(MESH:Hemolysis) positiveCorrelation a(MESH:"Blood Transfusion") View Subject | View Object

The plasma hemoglobin levels at two and four hours after SRBC-transfusion were greater than the cell-free hemoglobin levels in the supernatant of the SRBCs before transfusion (Figure 1C, Supplemental Table I), providing evidence that hemolysis occurs in vivo during and after transfusion of SRBCs. PubMed:27515135

Appears in Networks:
Annotations
MeSH
Hemorrhage
Text Location
Results

path(MESH:Hemolysis) increases p(HGNC:TNF) View Subject | View Object

Second, immune hemolysis is accompanied by production of TNF- which induces tissue factor expression in endothelial cells and also decreases the endothelial expression of thrombomodulin, a potent modulator of thrombin activity [62]. PubMed:28458720

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Veins
MeSH
beta-Thalassemia
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation path(MESH:Inflammation) View Subject | View Object

Furthermore, experiments of nature that lead to increased levels of chronic hemolysis, such as sickle cell anemia and paroxysmal nocturnal hemoglobinuria, provide evidence that low levels of hemolysis may be harmful, and contribute to inflammation, thrombosis, vasculopathy, and impaired host defenses against infection.1,11 PubMed:29603246

Appears in Networks:
Annotations
MeSH
Anemia, Sickle Cell
Text Location
Introduction

path(MESH:Hemolysis) positiveCorrelation path(MESH:Inflammation) View Subject | View Object

Thus, hemolysis can act as a kind of amplifier of the complex response to an infection or injury [8, 15] and worsen the outcome from animals and patients with systemic inflammation, sepsis, or trauma [1–4, 10]. PubMed:29956069

Appears in Networks:
Annotations
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation path(MESH:"Vascular Diseases") View Subject | View Object

Furthermore, experiments of nature that lead to increased levels of chronic hemolysis, such as sickle cell anemia and paroxysmal nocturnal hemoglobinuria, provide evidence that low levels of hemolysis may be harmful, and contribute to inflammation, thrombosis, vasculopathy, and impaired host defenses against infection.1,11 PubMed:29603246

Appears in Networks:
Annotations
MeSH
Anemia, Sickle Cell
Text Location
Introduction

path(MESH:Hemolysis) negativeCorrelation p(HGNC:CD59) View Subject | View Object

PIGA encodes a GPI biosynthesis protein, phosphatidylinositol N-acetylglucosaminyltransferase subunit A [5, 6], and erythrocytes deficient in GPI-anchored membrane proteins, including CD59, undergo complement-mediated hemolysis. PubMed:29929138

Appears in Networks:
Annotations
MeSH
Hemoglobinuria, Paroxysmal
Text Location
Introduction

path(MESH:Hemolysis) positiveCorrelation p(HGNC:CD59, var("p.Cys89Tyr")) View Subject | View Object

The Cys89Tyr mutation in CD59 was initially described with manifestation in infancy by chronic hemolysis and relapsing peripheral demyelinating disease resembling recurrent Guillain- Barre syndrome (GBS) or chronic inflammatory demyelinating polyneuropathy (CIDP). PubMed:29929138

Appears in Networks:
Annotations
MeSH
Hemoglobinuria, Paroxysmal
Text Location
Introduction

path(MESH:Hemolysis) positiveCorrelation path(MESH:Thrombophilia) View Subject | View Object

Intravascular hemolysis is one thrombophilic mechanisms in PNH (reviewed by Hill et al. [14]). PubMed:29929138

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
Cell Ontology (CL)
neutrophil
Cell Ontology (CL)
platelet
MeSH
Hemoglobinuria, Paroxysmal
Text Location
Discussion

path(MESH:Hemolysis) positiveCorrelation path(MESH:"Transfusion Reaction") View Subject | View Object

It is crucial, hence, to further investigate the mechanisms of sepsis-induced hemolysis with the aim of deriving possible therapeutic principles. Herein, we collected the most important previously known triggers of hemolysis during sepsis, which are (1) transfusion reactions and complement activation, (2) disseminated intravascular coagulation, (3) capillary stopped-flow, (4) restriction of glucose to red blood cells, (5) changes in red blood cell membrane properties, (6) hemolytic pathogens, and (7) red blood cell apoptosis. PubMed:29956069

Appears in Networks:
Annotations
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation bp(MESH:"Glucose-Galactose Malabsorption") View Subject | View Object

It is crucial, hence, to further investigate the mechanisms of sepsis-induced hemolysis with the aim of deriving possible therapeutic principles. Herein, we collected the most important previously known triggers of hemolysis during sepsis, which are (1) transfusion reactions and complement activation, (2) disseminated intravascular coagulation, (3) capillary stopped-flow, (4) restriction of glucose to red blood cells, (5) changes in red blood cell membrane properties, (6) hemolytic pathogens, and (7) red blood cell apoptosis. PubMed:29956069

Appears in Networks:
Annotations
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation path(MESH:Sepsis) View Subject | View Object

Both clinical [1–4] and experimental [5–8] studies have shown that sepsis and systemic inflammation lead to a massive release of hemoglobin from red blood cells (hemolysis) being accompanied with an increased risk of death [1–4, 8, 9]. PubMed:29956069

Appears in Networks:
Annotations
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation path(MESH:"Shock, Traumatic") View Subject | View Object

Thus, hemolysis can act as a kind of amplifier of the complex response to an infection or injury [8, 15] and worsen the outcome from animals and patients with systemic inflammation, sepsis, or trauma [1–4, 10]. PubMed:29956069

Appears in Networks:
Annotations
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation bp(MESH:"Blood Group Incompatibility") View Subject | View Object

Most hemolytic transfusion reactions^ can be attributed to ABO antibodies (ABO incompatibility of red blood cells) leading to intravascular hemolysis [69, 70] as a consequence of robust complement activation [71]. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
hepatocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation bp(HM:"Rh incompatibility") View Subject | View Object

Extravascular hemolysis, however, results from Rh incompatibility of red blood cells [72] and is complement independent [71]. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

path(MESH:Hemolysis) association path(HP:"Paroxysmal nocturnal hemoglobinuria") View Subject | View Object

Inhibition of the terminal complement cascade by eculizumab (inhibits the cleavage of C5 into C5a und C5b and thus the formation of the membrane attack complex 8, MAC C5b-C9) for the treatment of hemolytic paroxymal nocturnal hemoglobinuria (PNH) significantly prevented PNH-related symptoms in patients including abnormal thrombophilia, red blood cell destruction, and the extent of hemolysis [76]. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation a(CHEBI:Thrombin) View Subject | View Object

However, 6 years later, Heyes and co-workers demonstrated in an experimental study in rats that infusions of thrombin induce DIC accompanied with hemolysis and schistocytosis [89]. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Adenocarcinoma
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation a(HM:"fibrin deposition") View Subject | View Object

This study further supports the concept that fibrin deposition in the blood vessels as a result of DIC might contribute to red blood cell fragmentation and, in turn, hemolysis [89]. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Disseminated Intravascular Coagulation
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation path(HM:"renal stasis") View Subject | View Object

There are various studies that show a relationship between microvascular stasis and intravascular hemolysis. Already in 1940, Mumme described that renal stasis causes hemolysis [108]. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Microvessels
MeSH
Disseminated Intravascular Coagulation
Text Location
Review

path(MESH:Hemolysis) negativeCorrelation a(CHEBI:glucose) View Subject | View Object

Without sufficient glucose supply, red blood cells will starve and perish and cytoplasmic components will release. Hemolysis will be the consequence [120]. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Disseminated Intravascular Coagulation
Text Location
Review

path(MESH:Hemolysis) negativeCorrelation a(CHEBI:glucose) View Subject | View Object

Recently, our own collaboration could show that moderate glucose supply reduces hemolysis in rats treated with LPS to induce systemic inflammation [121]. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Disseminated Intravascular Coagulation
Text Location
Review

path(MESH:Hemolysis) negativeCorrelation a(CHEBI:lecithin) View Subject | View Object

Already in 1941, Macfarlane and collaborators described hemolysis due to loss of lecithin from the red blood cell membrane in consequence of an infection with Clostridium perfingens [128, 130]. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation a(HM:cytolysin) View Subject | View Object

Some pathogens are capable of causing hemolysis by cytolytic toxins. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

path(MESH:Hemolysis) positiveCorrelation p(HGNC:SLC48A1) View Subject | View Object

We show that the zebrafish kidney is the primary organ for heme-iron recycling during EP and that zebrafish Hrg1a and Hrg1b are heme transporters that are expressed and upregulated in kidney macrophages after PHZ-induced hemolysis. PubMed:30248094

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Kidney
Text Location
Results

path(MESH:Hemolysis) positiveCorrelation p(HGNC:HAMP) View Subject | View Object

Our results show that hamp1 levels are significantly elevated in the presence of PHZ but is equivalent in both, WT and DKO fish (S6 Fig). PubMed:30248094

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Kidney
Text Location
Results

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.