SARS-CoV-2, by binding to the angiotensin-converting enzyme 2 (ACE2) receptor in the lungs, may infect alveolar epithelial cells, vascular endothelial cells, and macrophages, leading to extensive apoptosis and vascular leakage caused by rapid and extensive viral replication evolving into acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) [44]. Here, ACE2 is linked to acute respiratory distress syndrome.