Role and mechanism of angiotensin‐converting enzyme 2 in acute lung injury in coronavirus disease 2019

Chronic Diseases and Translational Medicine - Tập 6 - Trang 98-105 - 2020
Meng-Yuan Liu1,2,3, Bo Zheng1,2,3, Yan Zhang1,2,3, Jian-Ping Li1,2,3
1Department of Cardiology,Peking University First Hospital, Beijing 100034, China
2NHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing 100034, China
3Key Laboratory of Molecular Cardiovascular Sciences of Ministry of Education, Health Science Center, Peking University, Beijing 100034, China

Tóm tắt

AbstractCoronavirus disease 2019 is a major threat to public health globally. Though its pathogenesis has not been fully elucidated, angiotensin‐converting enzyme 2 (ACE2) has been recently identified as a receptor for the entry of severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) into the cell. Here, we aimed to clarify the potential role of ACE2 in SARS‐CoV‐2‐induced acute lung injury and its underlying mechanism. As a receptor for coronavirus, ACE2 mediates the entry of SARS‐CoV‐2 into cells in a similar way as for severe acute respiratory syndrome coronavirus (SARS‐CoV). The high binding affinity of SARS‐CoV‐2 to ACE2 correlates with its efficient spread among humans. On the other hand, ACE2 negatively regulates the renin‐angiotensin‐aldosterone system (RAAS) primarily by converting angiotensin II to angiotensin 1–7, which exerts a beneficial effect on coronavirus‐induced acute lung injury. Human recombinant ACE2 has been considered as a potential therapy for SARS‐CoV‐2 by blocking virus entry and redressing the imbalance of RAAS in SARS‐CoV‐2 infection. The level of ACE2 expression can be upregulated by treatment with an ACE inhibitor (ACEI) or angiotensin Ⅱ type 1 receptor blocker (ARB). To date, no evidence shows that ACEIs or ARBs increase the susceptibility and mortality of patients infected with SARS‐CoV‐2, and hence, it is not advisable to discontinue such drugs in patients with cardiovascular disease.

Tài liệu tham khảo

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Chronic Diseases and Translational Medicine

Tập 6

98-105

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