Key result
In a systematic review of 27 animal studies, the majority reported increased ACE2 levels in response to ACEI or ARB treatment.
Why the study?
ACE2 facilitates SARS-CoV-2 cellular entry but protects against lung injury, and ACEIs/ARBs may upregulate ACE2 expression in experimental models.
Does ACEI/ARB administration affect ACE2 expression in experimental animal models?
Systematic Review (n=27)
Does ACEI/ARB administration affect ACE2 expression in experimental animal models?
In animal models, ACEI/ARB treatment generally upregulates ACE2 expression, which has implications for both SARS-CoV-2 viral entry and protection against lung injury.
Potential dual effects on SARS-CoV-2 entry and lung protection via ACE2; extends preclinical data but leaves human translation open.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the pathogen of coronavirus disease 2019 (COVID-19), caused the outbreak escalated to pandemic. Reports suggested that near 1-3% of COVID-19 cases have a fatal outcome. Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) are widely used in hypertension, heart failure and chronic kidney disease. These drugs have been reported to upregulate angiotensin converting enzyme 2 (ACE2) which produces Ang (1-7), the main counter-regulatory mediator of angiotensin II. This enzyme is also known as the receptor of SARS-CoV-2 promoting the cellular uptake of the virus in the airways, however, ACE2 itself proved to be protective in several experimental models of lung injury. The present study aimed to systematically review the relationship between ACEI/ARB administration and ACE2 expression in experimental models. After a comprehensive search and selection, 27 animal studies investigating ACE2 expression in the context of ACEI and ARB were identified. The majority of these papers reported increased ACE2 levels in response to ACEI/ARB treatment. This result should be interpreted in the light of the dual role of ACE2 being a promoter of viral entry to cells and a protective factor against oxidative damage in the lungs.
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Kriszta et al. (2021) conducted a systematic review in ACE2 expression in experimental models (n=27). Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) was evaluated on ACE2 expression levels. In a systematic review of 27 animal studies, the majority reported increased ACE2 levels in response to ACEI or ARB treatment.
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