1. Introduction
Since the start of the latest coronavirus (SARS-CoV-2) outbreak, the number of asymptomatic infected individuals and cases of coronavirus disease (COVID-19) have been increasing exponentially worldwide, which has been the biggest global health threat after world war II. COVID-19 is like to severe acute respiratory syndrome and mainly affects the respiratory tract and can subsequently result in acute respiratory distress syndrome (ARDS) and multi-organ failure(Huang et al. , 2020). Studies have proved that SARS-CoV-2, like SARS-CoV, is a family member of beta coronaviruses(Wang et al. , 2020) and 96% identical at the whole-genome level to a bat coronavirus(Zhou et al. , 2020). Meanwhile, the SARS-CoV-2 virus has been reported that it uses angiotensin converting enzyme-2 (ACE2) as a cellular entry receptor via the spike protein (S). The interesting thing is that SARS-CoV-2 binds ACE2 with higher affinity than SARS-CoV(Wrapp et al. , 2020), which meant that it is difficult to control. ACE2 is a key modulator of the renin-angiotensin-aldosterone system (RAAS), which is associated with blood pressure homeostasis, oxidative stress, vasoconstriction, fibrosis and inflammation(Turneret al. , 2002). The infection of SARS-CoV-2 may decrease the ACE2 expression and subsequently induce the inflammation in various organs. Moreover, accumulating evidence has demonstrated that ACE2 may be essential in the progression and clinical outcomes of COVID-19(Xuet al. , 2020). Therefore, we will review the role of ACE2 in various conditions, and discuss its potential implication in the susceptibility and progression of COVID-19.