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path(HM:"endothelial lesions")

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Entity

Name
endothelial lesions
Namespace
HM
Namespace Version
None
Pattern
.*

Appears in Networks 1

Heme Curation v0.0.1-dev

Mechanistic knowledge surrounding heme

In-Edges 4

a(CHEBI:heme) positiveCorrelation path(HM:"endothelial lesions") View Subject | View Object

Endothelial injury may also be related to Free hemoglobin and its breakdown oxidative product heme, and MPs, which mediates direct proinflammatory, proliferative, and pro-oxidant effects on endothelial cells [22–24] both in PNH and congenital CD59 deficiency, but may be more pronounced in congenital CD59 deficiency and perhaps even more in the brain due to loss of CD59 in the endothelium of these patients. PubMed:29929138

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

a(MESH:"Cell-Derived Microparticles") positiveCorrelation path(HM:"endothelial lesions") View Subject | View Object

Endothelial injury may also be related to Free hemoglobin and its breakdown oxidative product heme, and MPs, which mediates direct proinflammatory, proliferative, and pro-oxidant effects on endothelial cells [22–24] both in PNH and congenital CD59 deficiency, but may be more pronounced in congenital CD59 deficiency and perhaps even more in the brain due to loss of CD59 in the endothelium of these patients. PubMed:29929138

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

p(HGNC:HBB) positiveCorrelation path(HM:"endothelial lesions") View Subject | View Object

Endothelial injury may also be related to Free hemoglobin and its breakdown oxidative product heme, and MPs, which mediates direct proinflammatory, proliferative, and pro-oxidant effects on endothelial cells [22–24] both in PNH and congenital CD59 deficiency, but may be more pronounced in congenital CD59 deficiency and perhaps even more in the brain due to loss of CD59 in the endothelium of these patients. PubMed:29929138

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

p(HGNC:F3) positiveCorrelation path(HM:"endothelial lesions") View Subject | View Object

Injured endothelium may provide tissue factors and additional prothrombotic factors [21] that are not a prothrombotic mechanism in PNH. PubMed:29929138

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

Out-Edges 8

path(HM:"endothelial lesions") positiveCorrelation p(HGNC:F3) View Subject | View Object

Injured endothelium may provide tissue factors and additional prothrombotic factors [21] that are not a prothrombotic mechanism in PNH. PubMed:29929138

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

path(HM:"endothelial lesions") positiveCorrelation p(HGNC:HBB) View Subject | View Object

Endothelial injury may also be related to Free hemoglobin and its breakdown oxidative product heme, and MPs, which mediates direct proinflammatory, proliferative, and pro-oxidant effects on endothelial cells [22–24] both in PNH and congenital CD59 deficiency, but may be more pronounced in congenital CD59 deficiency and perhaps even more in the brain due to loss of CD59 in the endothelium of these patients. PubMed:29929138

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

path(HM:"endothelial lesions") positiveCorrelation a(CHEBI:heme) View Subject | View Object

Endothelial injury may also be related to Free hemoglobin and its breakdown oxidative product heme, and MPs, which mediates direct proinflammatory, proliferative, and pro-oxidant effects on endothelial cells [22–24] both in PNH and congenital CD59 deficiency, but may be more pronounced in congenital CD59 deficiency and perhaps even more in the brain due to loss of CD59 in the endothelium of these patients. PubMed:29929138

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

path(HM:"endothelial lesions") positiveCorrelation a(MESH:"Cell-Derived Microparticles") View Subject | View Object

Endothelial injury may also be related to Free hemoglobin and its breakdown oxidative product heme, and MPs, which mediates direct proinflammatory, proliferative, and pro-oxidant effects on endothelial cells [22–24] both in PNH and congenital CD59 deficiency, but may be more pronounced in congenital CD59 deficiency and perhaps even more in the brain due to loss of CD59 in the endothelium of these patients. PubMed:29929138

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

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:"endothelial lesions") increases path(MESH:Thrombosis) 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:"endothelial lesions") increases path(MESH:"Disseminated Intravascular Coagulation") 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

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.