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a(MESH:"Erythrocytes, Abnormal")

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

Entity

Name
Erythrocytes, Abnormal
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 6

a(CHEBI:"phosphatidyl-L-serine") positiveCorrelation a(MESH:"Erythrocytes, Abnormal") View Subject | View Object

Phosphatidylserine externalization and shedding are mediated by increased cellular Ca-flux and play an important role in natural RBC senescence [44]. PubMed:28458720

Appears in Networks:
Annotations
MeSH
Veins
MeSH
Anemia, Sickle Cell
MeSH
beta-Thalassemia
Text Location
Review

a(CHEBI:"phosphatidyl-L-serine") positiveCorrelation a(MESH:"Erythrocytes, Abnormal") View Subject | View Object

Under conditions of apoptosis or RBC damage, such as high shear rates, inflammation, or oxidative stress, RBCs can lose membrane asymmetry and expose phosphatidylserine [43]. PubMed:28458720

Appears in Networks:
Annotations
MeSH
Veins
MeSH
Anemia, Sickle Cell
MeSH
beta-Thalassemia
Text Location
Review

a(HM:"shear stress") positiveCorrelation a(MESH:"Erythrocytes, Abnormal") View Subject | View Object

Under conditions of apoptosis or RBC damage, such as high shear rates, inflammation, or oxidative stress, RBCs can lose membrane asymmetry and expose phosphatidylserine [43]. PubMed:28458720

Appears in Networks:
Annotations
MeSH
Veins
MeSH
Anemia, Sickle Cell
MeSH
beta-Thalassemia
Text Location
Review

bp(MESH:"Clot Retraction") negativeCorrelation a(MESH:"Erythrocytes, Abnormal") View Subject | View Object

In contrast, RBCs impair contraction and reduce stiffness, while increasing the overall contractile stress generated by the platelet-fibrin meshwork [75, 76, 85]. PubMed:28458720

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

bp(MESH:"Oxidative Stress") positiveCorrelation a(MESH:"Erythrocytes, Abnormal") View Subject | View Object

Under conditions of apoptosis or RBC damage, such as high shear rates, inflammation, or oxidative stress, RBCs can lose membrane asymmetry and expose phosphatidylserine [43]. PubMed:28458720

Appears in Networks:
Annotations
MeSH
Veins
MeSH
Anemia, Sickle Cell
MeSH
beta-Thalassemia
Text Location
Review

path(MESH:Inflammation) positiveCorrelation a(MESH:"Erythrocytes, Abnormal") View Subject | View Object

Under conditions of apoptosis or RBC damage, such as high shear rates, inflammation, or oxidative stress, RBCs can lose membrane asymmetry and expose phosphatidylserine [43]. PubMed:28458720

Appears in Networks:
Annotations
MeSH
Veins
MeSH
Anemia, Sickle Cell
MeSH
beta-Thalassemia
Text Location
Review

Out-Edges 9

a(MESH:"Erythrocytes, Abnormal") increases a(MESH:Arginase) View Subject | View Object

Damaged RBCs also release arginase that cleaves L-arginine, a substrate for NO production [29]. PubMed:28458720

Appears in Networks:
Annotations
MeSH
Veins
Text Location
Review

a(MESH:"Erythrocytes, Abnormal") increases p(HGNC:HBB) View Subject | View Object

When RBCs are damaged by high shear in continuous flow ventricular assist devices, free hemoglobin induces platelet aggregation, contributing to high risk of thrombotic complications [33]. PubMed:28458720

Appears in Networks:
Annotations
MeSH
Veins
MeSH
Acute Coronary Syndrome
Text Location
Review

a(MESH:"Erythrocytes, Abnormal") positiveCorrelation a(HM:"shear stress") View Subject | View Object

Under conditions of apoptosis or RBC damage, such as high shear rates, inflammation, or oxidative stress, RBCs can lose membrane asymmetry and expose phosphatidylserine [43]. PubMed:28458720

Appears in Networks:
Annotations
MeSH
Veins
MeSH
Anemia, Sickle Cell
MeSH
beta-Thalassemia
Text Location
Review

a(MESH:"Erythrocytes, Abnormal") positiveCorrelation bp(MESH:"Oxidative Stress") View Subject | View Object

Under conditions of apoptosis or RBC damage, such as high shear rates, inflammation, or oxidative stress, RBCs can lose membrane asymmetry and expose phosphatidylserine [43]. PubMed:28458720

Appears in Networks:
Annotations
MeSH
Veins
MeSH
Anemia, Sickle Cell
MeSH
beta-Thalassemia
Text Location
Review

a(MESH:"Erythrocytes, Abnormal") positiveCorrelation path(MESH:Inflammation) View Subject | View Object

Under conditions of apoptosis or RBC damage, such as high shear rates, inflammation, or oxidative stress, RBCs can lose membrane asymmetry and expose phosphatidylserine [43]. PubMed:28458720

Appears in Networks:
Annotations
MeSH
Veins
MeSH
Anemia, Sickle Cell
MeSH
beta-Thalassemia
Text Location
Review

a(MESH:"Erythrocytes, Abnormal") positiveCorrelation a(CHEBI:"phosphatidyl-L-serine") View Subject | View Object

Under conditions of apoptosis or RBC damage, such as high shear rates, inflammation, or oxidative stress, RBCs can lose membrane asymmetry and expose phosphatidylserine [43]. PubMed:28458720

Appears in Networks:
Annotations
MeSH
Veins
MeSH
Anemia, Sickle Cell
MeSH
beta-Thalassemia
Text Location
Review

a(MESH:"Erythrocytes, Abnormal") positiveCorrelation a(CHEBI:"phosphatidyl-L-serine") View Subject | View Object

Phosphatidylserine externalization and shedding are mediated by increased cellular Ca-flux and play an important role in natural RBC senescence [44]. PubMed:28458720

Appears in Networks:
Annotations
MeSH
Veins
MeSH
Anemia, Sickle Cell
MeSH
beta-Thalassemia
Text Location
Review

a(MESH:"Erythrocytes, Abnormal") decreases a(HM:"permeability of fibrin") View Subject | View Object

As a generality, incorporation of RBCs increases the lytic resistance and decreases the permeability of fibrin in a dose-dependent manner [79, 80]. PubMed:28458720

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

a(MESH:"Erythrocytes, Abnormal") negativeCorrelation bp(MESH:"Clot Retraction") View Subject | View Object

In contrast, RBCs impair contraction and reduce stiffness, while increasing the overall contractile stress generated by the platelet-fibrin meshwork [75, 76, 85]. PubMed:28458720

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

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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.