Since the ACE2 is highly expressed in pericytes, the patients infected with SARS-CoV-2 and predisposed with cardiac failure are more susceptible to develop severe cardiac problems [86]. The usage of mineralocorticoids receptor blocker can attenuates oxidative stress, reduces the level of ACE with the augmented production of the angiotensin 1–7 and attenuates the angiotensin II generation and increases the activity of ACE2 The antagonist of angiotensin II type 1 receptor, have modulates the profilin-1 expression and ACE2 [87]. The selective of the angiotensin II activity or synthesis mediated the augmented level of ACE2 expression and its activity in cardiac. Still, the combination of the lisinopril and losartan increases the activity of ACE2 but not ACE2 mRNA. The inhibition of ACE results in reduced formation of angiotensin II and metabolism of angiotensin 1–7, the angiotensin II type 1 receptor antagonist increases the metabolism of angiotensin II via ACE2 [88]. SARS-CoV 2 enters into the cell via the ACE2 receptor; this causes the decreased level of the ACE2 due to the binding of the spike protein to the ACE2 and no changes in ACE. This process causes the virus's entry, replicates it, and causes tissue injury via decreasing anti-atrophy, anti0-fibrosis, anti-inflammation, anti-oxidant, and vasodilation. On the other hand, the angiotensin II type 1 receptor causes pro-atrophy, pro-fibrosis, pro-inflammation, pro-oxidant, severe myocardial remodeling, vasoconstriction and vascular permeability which leads to tissue injury [89] (represented in Table 1).