Department of Pharmacology, School of Life Dentistry at Tokyo, The Nippon Dental University, Tokyo 102-0071, Japan.
Meikai University Research Institute of Odontology (M-RIO), Saitama 3500283, Japan.
Viruses. 2020 Apr 28;12(5):491. doi: 10.3390/v12050491.
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.
最近，由严重急性呼吸综合征冠状病毒 2 型（SARS-CoV-2）引起的疾病 COVID-19 已在全球范围内蔓延。近 20%的患者病情严重或危急。SARS-CoV-2 利用血管紧张素转换酶 2（ACE2）进入宿主细胞。ACE2 在肾素-血管紧张素-醛固酮系统（RAAS）中发挥重要作用，该系统调节血压和液体平衡。ACE2 还可以保护器官免受炎症损伤并调节肠道功能。ACE2 可被两种蛋白酶，即解整合素金属蛋白酶 17（ADAM17）和跨膜丝氨酸蛋白酶 2（TMPRSS2）切割。TMPRSS2 切割的 ACE2 允许 SARS-CoV-2 进入细胞，而 ADAM17 切割的 ACE2 为器官提供保护。SARS-CoV-2 感染引起的 ACE2 功能障碍使 COVID-19 恶化，并可能引发多器官衰竭。在这里，我们将解释 ACE2 在 COVID-19 严重和危急情况下发病机制中的作用，并讨论控制疾病的有利策略。
