tetano
Editor, Senior Moderator
Molecules
. 2020 Dec 31;26(1):E142.
doi: 10.3390/molecules26010142.
The Two-Way Switch Role of ACE2 in the Treatment of Novel Coronavirus Pneumonia and Underlying Comorbidities
Xiao Cong Pang[SUP] 1 2 [/SUP], Han Xu Zhang[SUP] 2 [/SUP], Zhi Zhang[SUP] 3 [/SUP], Suguro Rinkiko[SUP] 1 [/SUP], Yi Min Cui[SUP] 2 [/SUP], Yi Zhun Zhu[SUP] 1 4 [/SUP]
Affiliations
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.
Keywords: angiotensin-converting enzyme II (ACE2); hypertension; lung injury; renin-angiotensin system (RAS); severe acute respiratory syndrome (SARS).
. 2020 Dec 31;26(1):E142.
doi: 10.3390/molecules26010142.
The Two-Way Switch Role of ACE2 in the Treatment of Novel Coronavirus Pneumonia and Underlying Comorbidities
Xiao Cong Pang[SUP] 1 2 [/SUP], Han Xu Zhang[SUP] 2 [/SUP], Zhi Zhang[SUP] 3 [/SUP], Suguro Rinkiko[SUP] 1 [/SUP], Yi Min Cui[SUP] 2 [/SUP], Yi Zhun Zhu[SUP] 1 4 [/SUP]
Affiliations
- PMID: 33396184
- DOI: 10.3390/molecules26010142
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.
Keywords: angiotensin-converting enzyme II (ACE2); hypertension; lung injury; renin-angiotensin system (RAS); severe acute respiratory syndrome (SARS).