Key result
Severe COVID-19 promotes cardiac fibroblast differentiation, potentially driving long-term cardiac fibrosis and adverse remodeling.
Why the study?
Severe COVID-19 causes acute cardiac injury and adverse remodeling, but the emerging role of cardiac fibroblasts and myofibroblasts in SARS-CoV-2 cardiac complications requires further synthesis.
This review highlights the potential mechanisms by which COVID-19 exacerbates cardiovascular disease through cardiac fibroblast activation and subsequent fibrosis.
Answers are grounded in this paper and cite their sources.
May indicate need for fibrosis surveillance in severe COVID survivors; hypothesis-generating for fibroblast-targeted therapies.
Cardiovascular disease (CVD) is the leading cause of death worldwide. Current data suggest that patients with cardiovascular diseases experience more serious complications with coronavirus disease-19 (COVID-19) than those without CVD. In addition, severe COVID-19 appears to cause acute cardiac injury, as well as long-term adverse remodeling of heart tissue. Cardiac fibroblasts and myofibroblasts, being crucial in response to injury, may play a pivotal role in both contributing to and healing COVID-19-induced cardiac injury. The role of cardiac myofibroblasts in cardiac fibrosis has been well-established in the literature for decades. However, with the emergence of the novel coronavirus SARS-CoV-2, new cardiac complications are arising. Bursts of inflammatory cytokines and upregulation of TGF-β1 and angiotensin (AngII) are common in severe COVID-19 patients. Cytokines, TGF-β1, and Ang II can induce cardiac fibroblast differentiation, potentially leading to fibrosis. This review details the key information concerning the role of cardiac myofibroblasts in CVD and COVID-19 complications. Additionally, new factors including controlling ACE2 expression and microRNA regulation are explored as promising treatments for both COVID-19 and CVD. Further understanding of this topic may provide insight into the long-term cardiac manifestations of the COVID-19 pandemic and ways to mitigate its negative effects.
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Katwa et al. (2022) conducted a review in Cardiovascular disease and COVID-19. SARS-CoV-2 infection was evaluated. Severe COVID-19 induces inflammatory cytokines, TGF-β1, and Ang II, which can promote cardiac fibroblast differentiation and potentially lead to long-term cardiac fibrosis and adverse remodeling.
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