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*Correspondence: Jingxin Mo, [email protected] These authors have contributed equally to this work Disclaimer All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers

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When this happens, and additionally infection by SARS-CoV-2 downregulates ACE2 abundance on cell surfaces, as suggested by evidence from related coronaviruses [2], the result is the toxic overaccumulation of ANGII, exacerbated inflammation and, finally, acute respiratory distress syndrome and fulminant myocarditis (Figure 1)

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