Fig. 1
From: COVID-19 susceptibility: potential of ACE2 polymorphisms
Possible relation between renin-angiotensin system inhibition and COVID-19 [adapted from 19]. Competing hypothetical mechanisms by which use of ACEIs and ARBs might be harmful or protective in COVID-19. Hypothesis 1: SARS-CoV-2 enters cell by binding to ACE2. Use of ACEIs and ARBs could increase ACE2 abundance and enhance viral entry. Hypothesis 2: Ang II causes lung injury through inflammation and fibrosis upon activation of AT1R. Reduced production of Ang II by ACEIs or blockade of Ang II-AT1R interaction by ARBs increases generation of Ang (1-7) by ACE2 and activates Mas receptor (MasR) causing reduction in inflammation and fibrosis and thereby attenuating lung injury