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SARS-CoV-2 uses ACE-2 as a cellular input receptor, decreasing its expression and activity (Zhang et al. 2020), this may favor the ACE/Ang II/AT-1r axis. Therapeutic strategies can rebalance the ACE/ACE-2 balance in favor of the ACE-2/Ang(1–7)MASr axis with antifibrotic and antifibrotic effects in reducing COVID-19 lung lesions
