ROS in COVID-19 endothelial dysfunction (Homo sapiens)
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Description
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 Ma et. al..Quality Tags
Ontology Terms
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External references
DataNodes
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| Name | Type | Database reference | Comment |
|---|---|---|---|
| ACE2 (truncated) | GeneProduct | ENSG00000130234 (Ensembl)  | |
| ACE2 | GeneProduct | ENSG00000130234 (Ensembl) | |
| Angiotensin II | Metabolite | HMDB01035 (HMDB) | |
| ICAM1 | GeneProduct | ENSG00000090339 (Ensembl) | |
| IFN signaling | Pathway | ||
| IFNA1 | GeneProduct | ENSG00000197919 (Ensembl) | |
| IFNAR1 | GeneProduct | ENSG00000142166 (Ensembl) | |
| NFKB1 | GeneProduct | ENSG00000109320 (Ensembl) | |
| NOX1 | GeneProduct | NOX1 (HGNC) | |
| RAS signaling | Pathway | ||
| Reactive oxygen species | Metabolite | CHEBI:26523 (ChEBI) | |
| TNF | GeneProduct | ENSG00000232810 (Ensembl) | |
| TNFRSF1A | GeneProduct | ENSG00000067182 (Ensembl) | |
| nitric oxide | Metabolite | CHEBI:16480 (ChEBI) |
Annotated Interactions
No annotated interactions
