Interactions of coronaviruses with ACE2, angiotensin II, and RAS inhibitors—lessons from available evidence and insights into COVID-19
Open accessAbstract
The rapid spread of a novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has led to an ongoing pandemic of coronavirus disease 2019 (COVID-19). Recently, angiotensin-converting enzyme 2 (ACE2) has been shown to be a functional receptor for SARS-CoV-2 to enter host target cells. Given that angiotensin receptor blockers (ARBs) and an ACE inhibitor (ACEI) upregulated ACE2 expression in animal studies, the concern might arise regarding whether ARBs and ACEIs would increase the morbidity and mortality of COVID-19. On the other hand, animal data suggested a potential protective effect of ARBs against COVID-19 pneumonia because an ARB prevented the aggravation of acute lung injury in mice infected with SARS-CoV, which is closely related to SARS-CoV-2. Importantly, however, there is no clinical or experimental evidence supporting that ARBs and ACEIs either augment the susceptibility to SARS-CoV-2 or aggravate the severity and outcomes of COVID-19 at present. Until further data are available, it is recommended that ARB and ACEI medications be continued for the treatment of patients with cardiovascular disease and hypertension, especially those at high risk, according to guideline-directed medical therapy based on the currently available evidence.
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ACE2 enzyme expressed on the surface of cells is a COVID-19 receptor and is blocked or downregulated after binding of virus or even shed from the cell surface.
“The problem with the conversion of Ang II into Ang 1–7 is that the ACE2 enzyme expressed on surface of cells is a COVID-19 receptor and is blocked or downregulated after binding of virus or even shed from the cell surface [43].”
From Hyperactivation of P2X7 receptors as a culprit of COVID-19 neuropathology (2021) · cites this paper as [43]
In normal conditions, Ang II is converted by ACE2 into Ang 1-7.
“In normal conditions, Ang II is converted by the ACE2 receptor into angiotensin 1–7 (Ang 1–7) [43].”
From Hyperactivation of P2X7 receptors as a culprit of COVID-19 neuropathology (2021) · cites this paper as [43]
In rats with diabetic nephropathy, P2X7 receptor expression decreased ACE activity and Ang II levels, which might increase ACE2 expression and counteract SARS-CoV-2-induced inflammatory exacerbation.
“Furthermore, in rats with diabetic nephropathy, P2X7 receptor expression decreased ACE activity and Ang II levels [120], which might increase ACE2 expression [43] and counteract SARS-CoV-2-induced inflammatory exacerbation.”
From Hyperactivation of P2X7 receptors as a culprit of COVID-19 neuropathology (2021) · cites this paper as [43]
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References 43 · Cited by 426
- Authors
- Kai, H., & Kai, M.
- Affiliations
- Kurume University (JP)
- Fukuoka University (JP)
- Corresponding author
- Kai, Hisashi
- Venue
- Hypertension Research
- Published
- 2020-04-27
- Volume
- 43
- Issue
- 7
- Pages
- 648-654
- ISSN
- 0916-9636 (ISSN-L)
- 1348-4214
- PMC
- PMC7184165
- OpenAlex
- W3019849260
- Cited by
- 426
- References
- 43
- Citations by year
- 2026: 3 · 2025: 7 · 2024: 31 · 2023: 52 · 2022: 78 · 2021: 129 · 2020: 126
- FWCI
- 16.37
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Hypertension Research (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Japan Society for the Promotion of Science (19K08503)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
- Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
- Health Sciences › Medicine › Infectious Diseases › SARS-CoV-2 and COVID-19 Research
- Keywords
- SARS-CoV-2, COVID-19 pandemic, ACE2, angiotensin II, renin-angiotensin system, angiotensin receptor blockers, ACE inhibitors, drug interactions, COVID-19 severity, acute lung injury, hypertension, cardiovascular disease
- MeSH terms
- Betacoronavirus, Angiotensin-Converting Enzyme 2, COVID-19, SARS-CoV-2, Angiotensin II, Angiotensin-Converting Enzyme Inhibitors, Animals, Humans, Peptidyl-Dipeptidase A, Pneumonia, Viral, Coronavirus Infections, Angiotensin Receptor Antagonists, Pandemics
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