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. 2020 Apr 16;5(5):501–517. doi: 10.1016/j.jacbts.2020.04.003

Figure 1.

Figure 1

Interaction of CoVs With the RAS

Angiotensin-converting enzyme (ACE) converts angiotensin I (ANG1) (angiotensin 1-10) to angiotensin II (ANG2) (angiotensin 1-8), which is the major effector peptide of the renin-angiotensin system (RAS). ANG2 mediates its effects through selective interactions with G-protein–coupled angiotensin II type 1 receptor (AT1R) and G-protein–coupled angiotensin II type 1 type 2 receptor (AT2R). ANG2 is degraded to ANG-(1-7) by angiotensin-converting enzyme 2 (ACE2), ANG-(1-7) binds to the Mas receptor (not shown). The ACE2–ANG-(1-7)–Mas receptor axis opposes the effects of ACE–ANG2–AT1 axis. The binding of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike protein to ACE2 induces ACE2 shedding by activating a disintegrin and metalloproteinase-17 (ADAM-17). A decrease in ACE2 levels would be expected to result in a decrease in the levels ANG-(1-7) levels (cytoprotective) and a corresponding increase in tissue levels of ANG2 (proinflammatory and profibrotic). Transmembrane serine protease 2 (TMPRSS2), a type II cell membrane serine protease that activates the spike protein of SARS-CoV-2 and allows it to bind to ACE2. Modified from Simmons et al. (25). CoVs = coronaviruses; P = phosphorylation.