Sun M L, Yang J M, Sun Y P, Su G H
Department of Oncology, Jinan Central Hospital Affiliated to Shandong University, Jinan 250013, China.
The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese Ministry of Health and Chinese Academy of Medical Sciences, Department of Cardiology, Qilu Hospital of Shandong University, Jinan 250012, China.
Zhonghua Jie He He Hu Xi Za Zhi. 2020 Mar 12;43(3):219-222. doi: 10.3760/cma.j.issn.1001-0939.2020.03.016.
The novel coronavirus 2019 (COVID-19) infected patients by binding human ACE2, leading to severe pneumonia and highly mortality rate in patients. At present, there is no definite and effective treatment for COVID-19. ACE2 plays an important role in the RAS, and the imbalance between ACE/Ang II/AT1R pathway and ACE2/Ang (1-7)/Mas receptor pathway in the RAS system will lead to multi-system inflammation. Increased ACE and Ang II are poor prognostic factors for severe pneumonia. Animal studies have shown that RAS inhibitors could effectively relieve symptoms of acute severe pneumonia and respiratory failure. The binding of COVID-19 and ACE2 resulted in the exhaustion of ACE2, and then ACE2/Ang (1-7)/Mas receptor pathway was inhibited. The balance of the RAS system was broken, and this would lead to the exacerbation of acute severe pneumonia. Therefore, we speculate that ACEI and AT1R inhibitors could be used in patients with COVID-19 pneumonia under the condition of controlling blood pressure, and might reduce the pulmonary inflammatory response and mortality.
2019年新型冠状病毒（COVID-19）通过与人血管紧张素转换酶2（ACE2）结合来感染患者，导致患者出现严重肺炎且死亡率很高。目前，对于COVID-19尚无确切有效的治疗方法。ACE2在肾素-血管紧张素系统（RAS）中起重要作用，RAS系统中ACE/血管紧张素II（Ang II）/血管紧张素II 1型受体（AT1R）途径与ACE2/血管紧张素（1-7）/Mas受体途径之间的失衡会导致多系统炎症。ACE和Ang II升高是严重肺炎的不良预后因素。动物研究表明，RAS抑制剂可有效缓解急性重症肺炎和呼吸衰竭的症状。COVID-19与ACE2的结合导致ACE2耗竭，进而抑制了ACE2/Ang（1-7）/Mas受体途径。RAS系统的平衡被打破，这将导致急性重症肺炎加重。因此，我们推测在控制血压的情况下，血管紧张素转换酶抑制剂（ACEI）和AT1R抑制剂可用于COVID-19肺炎患者，可能会减轻肺部炎症反应并降低死亡率。
