Potential Roles of the Renin-Angiotensin System in the Pathogenesis and Treatment of COVID-19

Figure 1

Prehypertensin could cleave into Ang I in the presence of rennin, which then transformed into Ang II. Ang II would bind with the AT1R and AT2R, which then contributed to the tissue fibrosis and inflammation. Ang II deactivated by ACE2 could generate Ang 1-7 that could bind with the Mas receptor, which was involved in the anti-inflammation and antifibrosis. Angiotensin-converting enzyme inhibitor (ACEI)/ARB could inhibit the ACEI/Ang II/AT1 axis and eliminate the Ang II formation and the stimulation of AT1, which then attenuated the inflammatory reactions. The S protein could bind with ACE2, and then, the SARS-COV-2-ACE2 entered the cells, followed by membrane fusion. Then, the virus was released to the host cells. The decline of ACE2 and RAS imbalance would lead to inflammatory reactions. The ectogenous supplementation of hrsACE2 could block the entry of SARS-CoV-2 to host cells. The ACE2 level was normal, which showed protective effects to the hosts.