ROS in COVID-19 endothelial dysfunction (WP5258)

Homo sapiens

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Proposed mechanism for COVID-19 induced endothelial dysfunction via ROS, as described by Ma et Al. (2022). TNF-α stimulation of NADPH oxidase leads to accumulation of reactive oxygen species (ROS). Increased levels of IFN reduces the expression of functional ACE2, which leads to increased ROS via imbalanced RAS signaling. Excessive ROS disturbs vascular tone and increases endothelial permeability. Description modified from [https://europepmc.org/article/MED/34838588 Ma et. al.].

Authors

EAD2022 , Egon Willighagen , Eric Weitz , Kristina Hanspers , Martina Summer-Kutmon , and Aishwarya Iyer

Activity

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Organisms

Homo sapiens

Communities

Annotations

Pathway Ontology

disease pathway infectious disease pathway

Cell Type Ontology

endothelial cell

Disease Ontology

COVID-19

Participants
Query Drugst.One

Label Type Compact URI Comment
Nitric oxide Metabolite chebi:16480
Angiotensin II Metabolite hmdb:HMDB01035
Reactive oxygen species Metabolite chebi:26523
IFNAR1 GeneProduct ensembl:ENSG00000142166
TNFRSF1A GeneProduct ensembl:ENSG00000067182
ICAM1 GeneProduct ensembl:ENSG00000090339
NOX1 GeneProduct hgnc.symbol:NOX1
TNF GeneProduct ensembl:ENSG00000232810
ACE2 GeneProduct ensembl:ENSG00000130234
NFKB1 GeneProduct ensembl:ENSG00000109320
IFNA1 GeneProduct ensembl:ENSG00000197919
ACE2 (truncated) GeneProduct ensembl:ENSG00000130234

References

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