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path(MESH:"Reperfusion Injury")

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Entity

Name
Reperfusion Injury
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 3

a(CHEBI:heme) positiveCorrelation path(MESH:"Reperfusion Injury") View Subject | View Object

The consequences of heme toxicity can be appreciated in hemolytic diseases such as β-thalassemia, sickle-cell disease (SCD), ischemia-reperfusion (IR), and malaria (Katori et al., 2002; Pamplona et al., 2007;Vinchi et al., 2013). PubMed:24904418

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Text Location
Review

a(CHEBI:heme) positiveCorrelation path(MESH:"Reperfusion Injury") View Subject | View Object

The released heme can activate the innate immune pattern recognition receptor toll-like receptor 4 (TLR4) on inflammatory cells, platelets and endothelium, promoting a pro-inflammatory and pro-coagulant phenotype, ultimately leading to vaso-occlusion, ischemia-reperfusion physiology, tissue injury, and pain in murine models of SCD [5, 7±10]. PubMed:29694434

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

a(MESH:"Reactive Oxygen Species") positiveCorrelation path(MESH:"Reperfusion Injury") View Subject | View Object

Excess production of reactive oxygen species (ROS) has been implicated in progression of chronic heart failure as well as in other cardiovascular disorders including ischemia-reperfusion injury and cardiovascular complications of hemolytic diseases [2-7]. PubMed:28400318

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Text Location
Introduction

Out-Edges 3

path(MESH:"Reperfusion Injury") positiveCorrelation a(CHEBI:heme) View Subject | View Object

The consequences of heme toxicity can be appreciated in hemolytic diseases such as β-thalassemia, sickle-cell disease (SCD), ischemia-reperfusion (IR), and malaria (Katori et al., 2002; Pamplona et al., 2007;Vinchi et al., 2013). PubMed:24904418

Appears in Networks:
Annotations
Text Location
Review

path(MESH:"Reperfusion Injury") positiveCorrelation a(CHEBI:heme) View Subject | View Object

The released heme can activate the innate immune pattern recognition receptor toll-like receptor 4 (TLR4) on inflammatory cells, platelets and endothelium, promoting a pro-inflammatory and pro-coagulant phenotype, ultimately leading to vaso-occlusion, ischemia-reperfusion physiology, tissue injury, and pain in murine models of SCD [5, 7±10]. PubMed:29694434

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

path(MESH:"Reperfusion Injury") positiveCorrelation a(MESH:"Reactive Oxygen Species") View Subject | View Object

Excess production of reactive oxygen species (ROS) has been implicated in progression of chronic heart failure as well as in other cardiovascular disorders including ischemia-reperfusion injury and cardiovascular complications of hemolytic diseases [2-7]. PubMed:28400318

Appears in Networks:
Annotations
Text Location
Introduction

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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.