The new coronavirus was first reported in 2019 (China) and officially announced by the World Health
Organization as a pandemic in March 2020. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the
causative agent of the pneumonia-associated illnesses and shares structural homology with the related Severe acute
respiratory syndrome coronavirus-1 (SARS-CoV-1). One of the mechanisms for SARS-Cov-1 and -2 infection is mediated
by the angiotensin-converting enzyme-2 (ACE2) cell receptor, enabling the virus to enter the host cells. ACE2 is an isoform
of the angiotensin-converting enzyme 1 (ACE). The actions of ACE2 counterbalance the classic renin-angiotensin system
(RAS) axis through the production of Ang 1-7, which promotes cardiovascular, renal, and lung-protective effects. The
ACE2 is not the only route for SARS-CoV-2 to enter the host cells. However, due to its roles in the RAS and its
participation in the SARS-CoV-2 virulence, ACE2 has gained attention regarding viral mechanisms of pathogenesis, effects
of drugs that interfere with the RAS, and as a potential target for therapeutic strategies for the damages caused by SARSCoV-2 infection. Among other tissues, ACE2 gene expression seems to be increased in the lungs upon SARS-CoV-2
infection; however, amid other variables, expression and/or activity of ACE2 is shown as a disease, sex, and age-dependent.
The present review covers critical aspects for a comprehensive understanding of ACE2 and its current involvement in
SARS-CoV-2 infection and the development of COVID-19.