PMC:7652766 / 21979-22687 JSONTXT

{"target":"http://pubannotation.org/docs/sourcedb/PMC/sourceid/7652766","sourcedb":"PMC","sourceid":"7652766","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7652766","text":"Therefore, considering that SARS-CoV-2 uses ACE2 to enter cells, the main hypothesis of pulmonary pathology is that the increased activity of ACE (Ang-II) over ACE2 (Ang-1-7) may cause acute lung injury since the binding of the S protein to ACE2 leads to its blockage. Thus, the suppression of ACE2 occurs due to the increased internalization and release of ACE2 from the cell surface, which leads to a decrease in tissue ACE2 and the generation of Ang-1-7, and consequently higher Ang-II levels. Because of this, as shown in an experimental SARS-CoV-1 model, this process can drive an Ang II-AT1R-mediated inflammatory response in the lungs and potentially induce direct parenchymal injury (67, 80, 86, 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