Abstract
The renin–angiotensin system (RAS) is crucially involved in the physiology and pathology of all organs in mammals. Angiotensin-converting enzyme 2 (ACE2), which is a homolog of ACE, acts as a negative regulator in the homeostasis of RAS. ACE2 has been proven to be the receptor of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which caused the coronavirus disease 2019 (COVID-19) pandemic. As SARS-CoV-2 enters the host cells through binding of viral spike protein with ACE2 in humans, the distribution and expression level of ACE2 may be critical for SARS-CoV-2 infection. Growing evidence shows the implication of ACE2 in pathological progression in tissue injury and several chronic conditions such as hypertension, diabetes, and cardiovascular disease; this suggests that ACE2 is essential in the progression and clinical prognosis of COVID-19 as well. Therefore, we summarized the expression and activity of ACE2 under various conditions and regulators. We further discussed its potential implication in susceptibility to COVID-19 and its potential for being a therapeutic target in COVID-19.
Highlights
Coronavirus disease 2019 (COVID-19) is an acute respiratory disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) [1]
Clinical research has indicated a direct link between the downregulation of tissue Angiotensin-converting enzyme 2 (ACE2) and the imbalance of the renin–angiotensin system (RAS) in patients with COVID-19, which promotes the development of multiorgan injuries caused by SARS-CoV-2 infection [12]
Since the discovery of ACE2, progress has been made in elucidating its biochemical actions and fundamental role in cardiovascular diseases and as a receptor for SARS-CoV-2 attachment
Summary
Coronavirus disease 2019 (COVID-19) is an acute respiratory disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) [1] It was first reported in December 2019 in Wuhan, Hubei Province of China; as of March 24, 2021, it has resulted in more than 100 million infections and 3.48 million deaths worldwide. Clinical research has indicated a direct link between the downregulation of tissue ACE2 and the imbalance of the RAS in patients with COVID-19, which promotes the development of multiorgan injuries caused by SARS-CoV-2 infection [12]. Because of the crucial role of ACE2 in SARS-CoV-2 infection, potential therapeutic strategies include the prevention of the binding of human ACE2 and the receptor-binding domain of the viral spike protein or the direct and indirect regulation of ACE2 expression, small molecule inhibitors, drugs, ACE2 antibodies, or single-chain antibody fragments against ACE2, which may influence its activity. We summarize the regulation of ACE2 expression and activity under various conditions and regulators and discuss its role as a potential therapeutic target in COVID-19
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