curs 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, 87).
Another hypothesis states th