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by Wentao Ni, Xiuwen Yang, Deqing Yang, Jing Bao, Ran Li,
Yongjiu Xiao, Chang Hou, Haibin Wang, Jie Liu, Donghong Yang, Yu Xu, Zhaolong
Cao and Zhancheng Gao
Abstract
An outbreak of pneumonia caused by severe acute respiratory
syndrome coronavirus 2 (SARS-CoV-2) that started in Wuhan, China, at the end of
2019 has become a global pandemic. Both SARS-CoV-2 and SARS-CoV enter host
cells via the angiotensin-converting enzyme 2 (ACE2) receptor, which is
expressed in various human organs. We have reviewed previously published
studies on SARS and recent studies on SARS-CoV-2 infection, named coronavirus
disease 2019 (COVID-19) by the World Health Organization (WHO), confirming that
many other organs besides the lungs are vulnerable to the virus. ACE2 catalyzes
angiotensin II conversion to angiotensin-(1–7), and the
ACE2/angiotensin-(1–7)/MAS axis counteracts the negative effects of the
renin-angiotensin system (RAS), which plays important roles in maintaining the
physiological and pathophysiological balance of the body. In addition to the
direct viral effects and inflammatory and immune factors associated with
COVID-19 pathogenesis, ACE2 downregulation and the imbalance between the RAS
and ACE2/angiotensin-(1–7)/MAS after infection may also contribute to multiple
organ injury in COVID-19. The SARS-CoV-2 spike glycoprotein, which binds to
ACE2, is a potential target for developing specific drugs, antibodies, and
vaccines. Restoring the balance between the RAS and ACE2/angiotensin-(1–7)/MAS
may help attenuate organ injuries.
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