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Fig. 1 | Human Genomics

Fig. 1

From: COVID-19 preclinical models: human angiotensin-converting enzyme 2 transgenic mice

Fig. 1

The role of the ACE2 and the adverse effect of SARS-CoV in the RAAS. Renin cleaves angiotensinogen into angiotensin I (Ang I), and the circulating Ang I is hydrolyzed to Ang II by ACE. Ang II activates the AT1R to lead the pro-atrophy, pro-fibrosis, pro-inflammation, pro-oxidant, vasoconstrictor response, and increase aldosterone synthesis. ACE2 directly hydrolyzes Ang I and Ang II to generate Ang1–9 and Ang1–7, respectively. Ang1–7 binds to the MasR which leads to the cellular signaling that opposite to the tissue injury effects of Ang II and does not stimulate aldosterone secretion. The SARS-CoV destroys the balance of RAAS by downregulating the ACE2 expression levels. Conclusively, the disproportion between AT1R and MasR axes in SARS-CoV infected patients contributes to the development of tissue injury and more severe inflammatory reactions

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