1. Catalog
  2. Nodes
  3. path(MESH:"Vascular System Injuries")

path(MESH:"Vascular System Injuries")

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

Entity

Name
Vascular System Injuries
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 13

a(CHEBI:"carbon monoxide") negativeCorrelation path(MESH:"Vascular System Injuries") View Subject | View Object

By-products of heme and iron metabolism, such as heme oxygenase-dependent generation of carbon monoxide (CO), have antioxidant and anti-inflammatory protective functions against iron-induced vascular damage (33); therefore we examined the impact of CO donors on collagen exposure and thrombus formation in the ex vivo vascular injury model. PubMed:19276082

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

a(CHEBI:"iron trichloride") positiveCorrelation path(MESH:"Vascular System Injuries") View Subject | View Object

High concentrations of FeCl3 induce profound injury to the vasculature, leading to endothelial denudation, and collagen and tissue factor exposure, leading to the rapid formation of vaso-occlusive thrombi. PubMed:19276082

Appears in Networks:
Annotations
Text Location
Introduction

a(CHEBI:"iron trichloride") positiveCorrelation path(MESH:"Vascular System Injuries") View Subject | View Object

As demonstrated in Fig. 1, topically exposing aorta in vivo (Fig. 1A) or ex vivo (Fig. 1B) to 6% FeCl3 resulted in major vascular injury as evidenced by endothelial denudation, collagen exposure, and the subsequent formation of arterial thrombi (Fig. 1D and supplemental Video 1). PubMed:19276082

Appears in Networks:
Annotations
Text Location
Introduction

a(CHEBI:"iron trichloride") positiveCorrelation path(MESH:"Vascular System Injuries") 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:heme) increases path(MESH:"Vascular System Injuries") View Subject | View Object

Heme may be implicated and contribute to the development of (i) bp(MESH: PubMed:26875449

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

bp(MESH:"Blood Transfusion") increases path(MESH:"Vascular System Injuries") View Subject | View Object

An increase in plasma cell-free Hb and vascular dysfunction also has been shown after transfusion of autologous RBCs with long storage duration to healthy human subjects.19,20,37 PubMed:27308950

Appears in Networks:
Annotations
MeSH
Plasma
Text Location
Discussion

p(HGNC:HBB) positiveCorrelation path(MESH:"Vascular System Injuries") 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) increases path(MESH:"Vascular System Injuries") View Subject | View Object

Free hemoglobin (Hb) triggered vascular damage occurs in many hemolytic diseases, such as sickle cell disease, with an unmet need for specific therapeutic interventions. PubMed:26475040

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

p(HGNC:HBB) increases path(MESH:"Vascular System Injuries") View Subject | View Object

Depending on the scale, rate, and site of hemolysis, the primary adverse effects triggered by free Hb are vascular dysfunction, oxidative tissue damage, and altered inflammatory response [1], PubMed:26475040

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

p(HGNC:HBB) increases path(MESH:"Vascular System Injuries") View Subject | View Object

Several studies in animals have supported the idea that infusion of free Hb, stored RBC supernatant (preservation solution + plasma), and Hb-containing microvesicles causes vasoconstriction, vascular dysfunction, and vascular injury.12,16–18 PubMed:27308950

Appears in Networks:
Annotations
MeSH
Arteries
Text Location
Introduction

p(MGI:Hmox1) negativeCorrelation path(MESH:"Vascular System Injuries") View Subject | View Object

Clinical studies have confirmed endothelial dysfunction and vasculopathy in a patient with HO-1 deficiency, and similarly, mice lacking HO-1 have increased vascular injury and thrombotic complications (43, 44). PubMed:19276082

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

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

rxn(reactants(a(CHEBI:superoxide), p(HGNC:HBB)), products(a(CHEBI:"hydrogen peroxide"))) positiveCorrelation path(MESH:"Vascular System Injuries") View Subject | View Object

Furthermore superoxide can react with Hb to produce hydrogen peroxide (H2O2), a well defined prooxidative molecule that causes vascular injury (1). PubMed:19276082

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

Out-Edges 8

path(MESH:"Vascular System Injuries") positiveCorrelation a(CHEBI:"iron trichloride") View Subject | View Object

High concentrations of FeCl3 induce profound injury to the vasculature, leading to endothelial denudation, and collagen and tissue factor exposure, leading to the rapid formation of vaso-occlusive thrombi. PubMed:19276082

Appears in Networks:
Annotations
Text Location
Introduction

path(MESH:"Vascular System Injuries") positiveCorrelation a(CHEBI:"iron trichloride") View Subject | View Object

As demonstrated in Fig. 1, topically exposing aorta in vivo (Fig. 1A) or ex vivo (Fig. 1B) to 6% FeCl3 resulted in major vascular injury as evidenced by endothelial denudation, collagen exposure, and the subsequent formation of arterial thrombi (Fig. 1D and supplemental Video 1). PubMed:19276082

Appears in Networks:
Annotations
Text Location
Introduction

path(MESH:"Vascular System Injuries") 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:"Vascular System Injuries") negativeCorrelation a(CHEBI:"carbon monoxide") View Subject | View Object

By-products of heme and iron metabolism, such as heme oxygenase-dependent generation of carbon monoxide (CO), have antioxidant and anti-inflammatory protective functions against iron-induced vascular damage (33); therefore we examined the impact of CO donors on collagen exposure and thrombus formation in the ex vivo vascular injury model. PubMed:19276082

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Aorta
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:"Vascular System Injuries") positiveCorrelation rxn(reactants(a(CHEBI:superoxide), p(HGNC:HBB)), products(a(CHEBI:"hydrogen peroxide"))) View Subject | View Object

Furthermore superoxide can react with Hb to produce hydrogen peroxide (H2O2), a well defined prooxidative molecule that causes vascular injury (1). PubMed:19276082

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

path(MESH:"Vascular System Injuries") negativeCorrelation p(MGI:Hmox1) View Subject | View Object

Clinical studies have confirmed endothelial dysfunction and vasculopathy in a patient with HO-1 deficiency, and similarly, mice lacking HO-1 have increased vascular injury and thrombotic complications (43, 44). PubMed:19276082

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

path(MESH:"Vascular System Injuries") 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

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.