Therefore, the improvement of pulmonary inflammation and fibrosis, the amelioration of right heart pressures and pulmonary congestion, and the upregulation of ACE2 expression are various factors that could lead to an improved pulmonary environment, making the spread of pulmonary infections and inflammation less likely (27).Additionally, the antagonistic impact of MRA on mineralocorticoid receptors in monocytes and macrophages may impede the infiltration and aggregation of activated macrophages, thereby mitigating COVID-19-induced pulmonary tissue injury (28–30). This evidence concerns the gene ACE2 and COVID-19.