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.