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Updated: Dec 13, 2025
Live Imaging and Quantification of Viral Infection in K18 hACE2 Transgenic Mice Using Reporter-Expressing Recombinant SARS-CoV-2
Published on: November 5, 2021
Focus on clinical practice: angiotensin-converting enzyme 2 and corona virus disease 2019: pathophysiology and
Francesco Barillà1, Pier Paolo Bassareo2, Giuseppe Calcaterra3
1Department of Clinical, Internal, Anesthesiological, and Cardiovascular Sciences, University of Rome 'Sapienza', Italy.
Abstract:
: ACE2 receptor has a broad expression pattern in the cellular membrane and provides a protective action against the development of cardiovascular diseases. Recently, this enzyme has become of extreme interest during the pandemic infection of COVID-19 (coronavirus disease 2019). This virus invades alveolar epithelium and cardiomyocytes using ACE2 as a transmembrane receptor. ACE2 is a counter-regulatory peptide that degrades Ang II into Ang 1-7, thereby attenuating the biological effects of the AT1 receptor. The binding between the spike protein of COVID-19 and the enzyme is crucial for the virus to enter the target cells, but whether an increase in ACE2 activity could facilitate the infection is not yet demonstrated. However, this aspect has raised many concerns about the use of ACE inhibitors or ARBs in infected patients or patients at risk of infection. It appears that cellular infection leads to a reduction in ACE2 expression and an increase in the activity of the Ang II--AT1 axis, which leads to the release of pro-inflammatory cytokines, ARDS, myocarditis, and hypercoagulability with the possibility of exacerbation of acute coronary syndrome, induction of pulmonary embolism, or appearance of disseminated intravascular coagulation. Therefore, ACE inhibitors or angiotensin receptor blocker drugs should be continued in infected patients, as their discontinuation can increase Ang II activity and induce injury to the lungs or cardiovascular system.
Insights
The angiotensin-converting enzyme 2 (ACE2) receptor plays a protective role in cardiovascular health but is used by SARS-CoV-2 for cell entry. Continued use of ACE inhibitors and ARBs is recommended for COVID-19 patients to prevent cardiovascular complications.
Area of Science:
- Cardiovascular Disease
- Infectious Disease
- Molecular Biology
Background:
- The angiotensin-converting enzyme 2 (ACE2) receptor is vital for cardiovascular protection by degrading Angiotensin II (Ang II).
- COVID-19 (coronavirus disease 2019) utilizes ACE2 as a transmembrane receptor for viral entry into alveolar epithelium and cardiomyocytes.
- Concerns exist regarding the use of ACE inhibitors and Angiotensin Receptor Blockers (ARBs) in COVID-19 patients due to ACE2's role.
Purpose of the Study:
- To investigate the role of ACE2 in COVID-19 infection and its implications for cardiovascular health.
- To clarify the impact of COVID-19 on ACE2 expression and the renin-angiotensin system (RAS).
- To provide guidance on the management of ACE inhibitors and ARBs in patients with or at risk of COVID-19.
Main Methods:
- Review of current literature on ACE2 function, COVID-19 pathogenesis, and cardiovascular implications.
- Analysis of the interaction between the SARS-CoV-2 spike protein and the ACE2 receptor.
- Examination of the effects of cellular infection on ACE2 expression and the Ang II-AT1 axis.
Main Results:
- COVID-19 infection leads to a reduction in ACE2 expression, increasing Ang II activity.
- This disruption of the ACE2-mediated protective axis promotes inflammation, ARDS, myocarditis, and hypercoagulability.
- Potential cardiovascular complications include exacerbation of acute coronary syndrome, pulmonary embolism, and disseminated intravascular coagulation.
Conclusions:
- Discontinuation of ACE inhibitors or ARBs in COVID-19 patients may worsen outcomes by increasing Ang II activity and inducing lung or cardiovascular injury.
- Continued use of ACE inhibitors and ARBs is recommended for infected patients to maintain cardiovascular and pulmonary protection.
- Understanding the ACE2-SARS-CoV-2 interaction is critical for managing cardiovascular comorbidities in the context of the pandemic.
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