[Inhibitors of RAS Might Be a Good Choice for the Therapy of COVID-19 Pneumonia]

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.
[Article in Chinese]


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.

新型冠状病毒通过与人体血管紧张素转化酶2(ACE2)结合感染产生重症肺炎,传染性强,病死率高,目前无确切有效的治疗方式。ACE2是肾素-血管紧张素系统(RAS)的重要组成部分,RAS系统中ACE/Ang II/AT1R通路与ACE2/Ang(1-7)/Mas受体通路失衡将导致多系统炎症。ACE和Ang II升高是重症肺炎的不良预后因素。动物实验结果显示,应用RAS抑制剂可以有效缓解急性重症肺炎症状,缓解呼吸衰竭。新型冠状病毒与ACE2的结合导致ACE2耗竭,ACE2/Ang (1-7)/Mas受体通路受到抑制,RAS系统失衡,使新型冠状病毒肺炎患者病死率升高。因此,在控制血压的情况下,对新型冠状病毒肺炎患者应用ACEI及AT1R抑制剂,有可能减轻患者肺部炎症反应,降低患者病死率。.

MeSH terms

  • Angiotensin II
  • Angiotensin-Converting Enzyme 2
  • Angiotensin-Converting Enzyme Inhibitors / therapeutic use*
  • Animals
  • Betacoronavirus* / drug effects
  • Betacoronavirus* / pathogenicity
  • Blood Pressure / drug effects
  • COVID-19
  • COVID-19 Drug Treatment
  • Coronavirus Infections / drug therapy*
  • Humans
  • Inflammation* / drug therapy
  • Inflammation* / etiology
  • Lung
  • Peptide Fragments
  • Peptidyl-Dipeptidase A* / drug effects
  • Peptidyl-Dipeptidase A* / physiology
  • Pneumonia, Viral / drug therapy*
  • Pneumonia, Viral / etiology
  • Prognosis
  • Renin-Angiotensin System* / drug effects
  • Renin-Angiotensin System* / physiology
  • SARS-CoV-2


  • Angiotensin-Converting Enzyme Inhibitors
  • Peptide Fragments
  • Angiotensin II
  • ACE protein, human
  • Peptidyl-Dipeptidase A
  • ACE2 protein, human
  • Angiotensin-Converting Enzyme 2