SPARQL | HTML5 RDFa and Microdata document
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http://purl.org/dc/elements/1.1/source http://purl.org/dc/elements/1.1/title
ACE2 inhibition leads to pulmonary fibrosis
http://purl.org/dc/terms/description
This AOP outlines how ACE-2 plays a detrimental role in causing fibrotic damage to the lung by influencing various factors such as fibrogenic components, proinflammatory cytokines, and a lack of oxygen. When the activity of ACE2 is suppressed, the conversion of Ang II into Ang-(1-7) is not properly facilitated. Consequently, the levels of proinflammatory Ang II rise, while the levels of anti-inflammatory Ang-(1-7) decrease. Notably, ACE2 inhibition has been observed to raise the levels of Ang II peptides, which are a ligand for the type 1 angiotensin receptor (AT1R). This phenomenon is considered a significant risk factor for lung fibrosis, vasoconstriction, endothelial dysfunction, and cell death.
http://purl.org/dc/terms/identifier http://purl.org/dc/terms/references
https://identifiers.org/pubmed/33677612
https://identifiers.org/pubmed/34095051
https://identifiers.org/pubmed/35032963
http://purl.org/spar/cito/cites
https://identifiers.org/pubmed/33677612
https://identifiers.org/pubmed/34095051
https://identifiers.org/pubmed/35032963
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