ACE2: The key Molecule for Understanding the Pathophysiology of Severe and Critical Conditions of COVID-19: Demon or Angel?
1
Department of Pharmacology, School of Life Dentistry at Tokyo, The Nippon Dental University, Tokyo 102-0071, Japan
2
Meikai University Research Institute of Odontology (M-RIO), Saitama 3500283, Japan
3
Faculty of Life Sciences, Prefectural University of Hiroshima, Hiroshima 7270023, Japan
*
Author to whom correspondence should be addressed.
Viruses 2020, 12(5), 491; https://doi.org/10.3390/v12050491
Received: 30 March 2020 / Revised: 24 April 2020 / Accepted: 27 April 2020 / Published: 28 April 2020
(This article belongs to the Special Issue Pathogenesis of Human and Animal Coronaviruses)
Recently, the SARS-CoV-2 induced disease COVID-19 has spread all over the world. Nearly 20% of the patients have severe or critical conditions. SARS-CoV-2 exploits ACE2 for host cell entry. ACE2 plays an essential role in the renin–angiotensin–aldosterone system (RAAS), which regulates blood pressure and fluid balance. ACE2 also protects organs from inflammatory injuries and regulates intestinal functions. ACE2 can be shed by two proteases, ADAM17 and TMPRSS2. TMPRSS2-cleaved ACE2 allows SARS-CoV-2 cell entry, whereas ADAM17-cleaved ACE2 offers protection to organs. SARS-CoV-2 infection-caused ACE2 dysfunction worsens COVID-19 and could initiate multi-organ failure. Here, we will explain the role of ACE2 in the pathogenesis of severe and critical conditions of COVID-19 and discuss auspicious strategies for controlling the disease.
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MDPI and ACS Style
Xiao, L.; Sakagami, H.; Miwa, N. ACE2: The key Molecule for Understanding the Pathophysiology of Severe and Critical Conditions of COVID-19: Demon or Angel? Viruses 2020, 12, 491.
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