ACE2: The Key Molecule for Understanding the Pathophysiology of Severe and Critical Conditions of COVID-19: Demon or Angel?
ACE2: The Key Molecule for Understanding the Pathophysiology of Severe and Critical Conditions of COVID-19: Demon or Angel?
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DOI：
10.3390/v12050491
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发表时间：
2020-05-01
期刊：
影响因子：
4.7
通讯作者：
Miwa, Nobuhiko
中科院分区：
文献类型：
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作者：
Xiao, Li;Sakagami, Hiroshi;Miwa, Nobuhiko
最近，由SARS-CoV-2引起的疾病COVID-19在全球范围内蔓延。近20%的患者病情严重或危重。SARS-CoV-2利用ACE 2进入宿主细胞。ACE 2在调节血压和体液平衡的肾素-血管紧张素-醛固酮系统（RAAS）中起重要作用。ACE 2还保护器官免受炎症损伤并调节肠道功能。ACE 2可由两种蛋白酶ADAM 17和TMPRSS 2脱落。TMPRSS 2切割的ACE 2允许SARS-CoV-2细胞进入，而ADAM 17切割的ACE 2提供对器官的保护。SARS-CoV-2感染引起的ACE 2功能障碍会导致COVID-19，并可能引发多器官衰竭。在这里，我们将解释ACE 2在COVID-19严重和危重疾病发病机制中的作用，并讨论控制该疾病的吉祥策略。
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.