Fig. 1
From: Identifying pathophysiological bases of disease in COVID-19
a Key pivotal modulating and antagonistic roles of ACE and ACE2 in the RAAS, and SARS-Cov-2 binding to ACE2 and TMPRSS2. ACE catalyzes the conversion of AngI into AngII, thereby inducing hypertensive and pro-inflammatory effects, while ACE2 mediates the formation of angiotensin-(1–9) from AngI. ACE2 also counters ACE activity by reducing AngII bioavailability and increasing Ang-(1–7) formation, which acts as a vasodilator and exerts antiinflammatory activities through Mas receptors. SARS-CoV-2 interacts and downregulates ACE-2. b In this context, an imbalance in ACE2/Ang-(1–7) and ACE/AngII axes would be critical in the development of severe COVID-19 symptomatology