tetano
Editor, Senior Moderator
Cells
. 2022 Apr 13;11(8):1316.
doi: 10.3390/cells11081316.
CVD and COVID-19: Emerging Roles of Cardiac Fibroblasts and Myofibroblasts
Laxmansa C Katwa[SUP] 1 [/SUP], Chelsea Mendoza[SUP] 1 [/SUP], Madison Clements[SUP] 1 [/SUP]
Affiliations
Abstract
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.
Keywords: COVID-19; TGF-β1; fibroblast; fibrosis; myofibroblast.
. 2022 Apr 13;11(8):1316.
doi: 10.3390/cells11081316.
CVD and COVID-19: Emerging Roles of Cardiac Fibroblasts and Myofibroblasts
Laxmansa C Katwa[SUP] 1 [/SUP], Chelsea Mendoza[SUP] 1 [/SUP], Madison Clements[SUP] 1 [/SUP]
Affiliations
- PMID: 35455995
- PMCID: PMC9031661
- DOI: 10.3390/cells11081316
Abstract
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.
Keywords: COVID-19; TGF-β1; fibroblast; fibrosis; myofibroblast.