Abstract
December 2019 saw the emergence of the coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), which has spread across the globe. The high infectivity and ongoing mortality of SARS-CoV-2 emphasize the demand of drug discovery. Angiotensin-converting enzyme II (ACE2) is the functional receptor for SARS-CoV-2 entry into host cells. ACE2 exists as a membrane-bound protein on major viral target pulmonary epithelial cells, and its peptidase domain (PD) interacts SARS-CoV-2 spike protein with higher affinity. Therefore, targeting ACE2 is an important pharmacological intervention for a SARS-CoV-2 infection. In this review, we described the two-way switch role of ACE2 in the treatment of novel coronavirus pneumonia and underlying comorbidities, and discussed the potential effect of the ACE inhibitor and angiotensin receptor blocker on a hypertension patient with the SARS-CoV-2 infection. In addition, we analyzed the S-protein-binding site on ACE2 and suggested that blocking hot spot-31 and hot spot-353 on ACE2 could be a therapeutic strategy for preventing the spread of SARS-CoV-2. Besides, the recombinant ACE2 protein could be another potential treatment option for SARS-CoV-2 induced acute severe lung failure. This review could provide beneficial information for the development of anti-SARS-CoV-2 agents via targeting ACE2 and the clinical usage of renin-angiotensin system (RAS) drugs for novel coronavirus pneumonia treatment.
Highlights
December 2019 saw the emergence of the coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), which emerged in Wuhan, Hubei province, in central China, and spread rapidly across the globe [1,2]
The cryo-electron microscopy structure of SARSCoV-2 and full-length human angiotensin-converting enzyme 2 (ACE2)-B0AT1 complex were analyzed [11,12]. These findings suggest ACE2 is a potential target for anti-SARS-CoV-2 agent development
Compared with kidney and intestinal epithelia, ACE2 is moderately expressed in the lung, but respiratory type II alveolar cells are the important sites of entrance for SARS-CoV-2, in particular, the abundant expression of ACE2 in type II pneumocytes may cause rapid viral expansion and local alveolar wall damage, resulting in further severe diffuse alveolar destruction [30]
Summary
December 2019 saw the emergence of the coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), which emerged in Wuhan, Hubei province, in central China, and spread rapidly across the globe [1,2]. Typical clinical features of SARS-CoV-2 infected patients are fever, dyspnea, dry cough, headache, and pneumonia, which are similar to the symptoms caused by human severe acute respiratory syndrome coronavirus (SARS-CoV) [5,6]. The cryo-electron microscopy (cryo-EM) structure of SARSCoV-2 and full-length human ACE2-B0AT1 complex were analyzed [11,12]. These findings suggest ACE2 is a potential target for anti-SARS-CoV-2 agent development. We reviewed the two-way switch role of ACE2 in the treatment of SARSCoV-2 pneumonia This could be informative for targeting the ACE2 therapeutic strategy and the clinical application of RAS drugs for SARS-CoV-2 therapy
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