Department of Pulmonary and Critical Care Medicine, Peking University People's Hospital, Beijing, China.
Department of Pulmonary and Critical Care Medicine, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Crit Care. 2020 Jul 13;24(1):422. doi: 10.1186/s13054-020-03120-0.
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. SARS-CoV-2 enters lung cells via the ACE2 receptor. The cell-free and macrophage-phagocytosed virus can spread to other organs and infect ACE2-expressing cells at local sites, causing multi-organ injury.
2019 年底，中国武汉爆发了由严重急性呼吸综合征冠状病毒 2（SARS-CoV-2）引起的肺炎疫情，现已成为全球性大流行。SARS-CoV-2 和 SARS-CoV 通过血管紧张素转换酶 2（ACE2）受体进入宿主细胞，该受体在各种人体器官中表达。我们对之前发表的关于 SARS 的研究和最近关于世界卫生组织（WHO）命名的 2019 年冠状病毒病（COVID-19）的 SARS-CoV-2 感染研究进行了综述，证实除肺部以外，许多其他器官也容易受到病毒侵害。ACE2 催化血管紧张素 II 转化为血管紧张素-(1-7)，ACE2/血管紧张素-(1-7)/MAS 轴抵消了肾素-血管紧张素系统（RAS）的负面效应，该系统在维持身体的生理和病理生理平衡方面发挥着重要作用。除了与 COVID-19 发病机制相关的病毒直接作用、炎症和免疫因素外，感染后 ACE2 下调以及 RAS 和 ACE2/血管紧张素-(1-7)/MAS 之间的失衡也可能导致 COVID-19 的多器官损伤。与 ACE2 结合的 SARS-CoV-2 刺突糖蛋白是开发特异性药物、抗体和疫苗的潜在靶点。恢复 RAS 和 ACE2/血管紧张素-(1-7)/MAS 之间的平衡可能有助于减轻器官损伤。SARS-CoV-2 通过 ACE2 受体进入肺细胞。无细胞和巨噬细胞吞噬的病毒可以传播到其他器官，并在局部部位感染 ACE2 表达细胞，导致多器官损伤。
