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Role of the Renin-Angiotensin System in Long COVID's Cardiovascular Injuries
Elena Cojocaru1, Cristian Cojocaru2, Cristiana-Elena Vlad3,4
1Morpho-Functional Sciences II Department, Faculty of Medicine, "Grigore T. Popa" University of Medicine and Pharmacy, 700115 Iasi, Romania.
Abstract:
The renin-angiotensin system (RAS) is one of the biggest challenges of cardiovascular medicine. The significance of the RAS in the chronic progression of SARS-CoV-2 infection and its consequences is one of the topics that are currently being mostly discussed. SARS-CoV-2 undermines the balance between beneficial and harmful RAS pathways. The level of soluble ACE2 and membrane-bound ACE2 are both upregulated by the endocytosis of the SARS-CoV-2/ACE2 complex and the tumor necrosis factor (TNF)-α-converting enzyme (ADAM17)-induced cleavage. Through the link between RAS and the processes of proliferation, the processes of fibrous remodelling of the myocardium are initiated from the acute phase of the disease, continuing into the long COVID stage. In the long term, RAS dysfunction may cause an impairment of its beneficial effects leading to thromboembolic processes and a reduction in perfusion of target organs. The main aspects of ACE2-a key pathogenic role in COVID-19 as well as the mechanisms of RAS involvement in COVID cardiovascular injuries are studied. Therapeutic directions that can be currently anticipated in relation to the various pathogenic pathways of progression of cardiovascular damage in patients with longCOVID have also been outlined.
Insights
The renin-angiotensin system (RAS) is implicated in cardiovascular damage during COVID-19. SARS-CoV-2 disrupts RAS balance, leading to myocardial fibrosis and organ dysfunction in long COVID patients.
Area of Science:
- Cardiovascular Medicine
- Infectious Diseases
- Molecular Biology
Background:
- The renin-angiotensin system (RAS) plays a critical role in cardiovascular homeostasis.
- SARS-CoV-2 infection significantly impacts RAS pathways, presenting a major challenge in cardiovascular medicine.
- Understanding RAS involvement in COVID-19 pathogenesis is crucial for managing cardiovascular complications.
Purpose of the Study:
- To investigate the role of the renin-angiotensin system (RAS) in the cardiovascular sequelae of SARS-CoV-2 infection.
- To elucidate the mechanisms by which SARS-CoV-2 disrupts RAS balance and contributes to cardiovascular injury.
- To explore potential therapeutic strategies targeting RAS dysfunction in long COVID.
Main Methods:
- Analysis of ACE2 regulation, including soluble and membrane-bound forms, in response to SARS-CoV-2.
- Investigation of the link between RAS activation and myocardial fibrous remodeling.
- Review of pathogenic pathways contributing to cardiovascular damage in acute and long COVID.
Main Results:
- SARS-CoV-2 disrupts the balance of beneficial and harmful RAS pathways.
- ACE2 levels are upregulated via SARS-CoV-2/ACE2 complex endocytosis and ADAM17-induced cleavage.
- RAS dysfunction contributes to myocardial fibrosis, thromboembolic events, and reduced organ perfusion in COVID-19 and long COVID.
Conclusions:
- The renin-angiotensin system is a key player in COVID-19-associated cardiovascular damage.
- Dysfunctional RAS contributes to both acute and chronic cardiovascular complications, including long COVID.
- Targeting specific RAS pathways offers potential therapeutic avenues for mitigating cardiovascular injury.
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