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Angiotensin II (ATII) interacts with AT1R receptor and induces ROS production via NADPH oxidase (NOX) in endothelial cells triggering mitochondrial oxidative stress and endothelial dysfunction. It is believed that SARS-CoV-2 S-protein binds to ACE2 causing its subsequent local or systemic depletion of this enzyme that cleaves ATII, which, in turn, increased ATII level.
