tetano
Editor, Senior Moderator
Chronic Dis Transl Med
. 2020 Jun;6(2):98-105.
doi: 10.1016/j.cdtm.2020.05.003. Epub 2020 May 19.
Role and Mechanism of Angiotensin-Converting Enzyme 2 in Acute Lung Injury in Coronavirus Disease 2019
Meng-Yuan Liu[SUP] 1 2 3 [/SUP], Bo Zheng[SUP] 1 2 3 [/SUP], Yan Zhang[SUP] 1 2 3 [/SUP], Jian-Ping Li[SUP] 1 2 3 [/SUP]
Affiliations
Abstract
Coronavirus 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.
Keywords: Acute lung injury; Angiotensin-converting enzyme 2; Severe acute respiratory syndrome coronavirus 2.
. 2020 Jun;6(2):98-105.
doi: 10.1016/j.cdtm.2020.05.003. Epub 2020 May 19.
Role and Mechanism of Angiotensin-Converting Enzyme 2 in Acute Lung Injury in Coronavirus Disease 2019
Meng-Yuan Liu[SUP] 1 2 3 [/SUP], Bo Zheng[SUP] 1 2 3 [/SUP], Yan Zhang[SUP] 1 2 3 [/SUP], Jian-Ping Li[SUP] 1 2 3 [/SUP]
Affiliations
- PMID: 32550040
- PMCID: PMC7236734
- DOI: 10.1016/j.cdtm.2020.05.003
Abstract
Coronavirus 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.
Keywords: Acute lung injury; Angiotensin-converting enzyme 2; Severe acute respiratory syndrome coronavirus 2.