CVD and COVID-19: Emerging Roles of Cardiac Fibroblasts and Myofibroblasts
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 injur...
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Format: | Article |
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MDPI AG
2022-04-01
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Series: | Cells |
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Online Access: | https://www.mdpi.com/2073-4409/11/8/1316 |
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author | Laxmansa C. Katwa Chelsea Mendoza Madison Clements |
author_facet | Laxmansa C. Katwa Chelsea Mendoza Madison Clements |
author_sort | Laxmansa C. Katwa |
collection | DOAJ |
description | 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. |
first_indexed | 2024-03-09T11:01:28Z |
format | Article |
id | doaj.art-b775cee339f74c86bc84c16d54161683 |
institution | Directory Open Access Journal |
issn | 2073-4409 |
language | English |
last_indexed | 2024-03-09T11:01:28Z |
publishDate | 2022-04-01 |
publisher | MDPI AG |
record_format | Article |
series | Cells |
spelling | doaj.art-b775cee339f74c86bc84c16d541616832023-12-01T01:14:13ZengMDPI AGCells2073-44092022-04-01118131610.3390/cells11081316CVD and COVID-19: Emerging Roles of Cardiac Fibroblasts and MyofibroblastsLaxmansa C. Katwa0Chelsea Mendoza1Madison Clements2Department of Physiology, Brody School of Medicine, East Carolina University, Greenville, NC 27834, USADepartment of Physiology, Brody School of Medicine, East Carolina University, Greenville, NC 27834, USADepartment of Physiology, Brody School of Medicine, East Carolina University, Greenville, NC 27834, USACardiovascular 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.https://www.mdpi.com/2073-4409/11/8/1316TGF-β1fibroblastmyofibroblastfibrosisCOVID-19 |
spellingShingle | Laxmansa C. Katwa Chelsea Mendoza Madison Clements CVD and COVID-19: Emerging Roles of Cardiac Fibroblasts and Myofibroblasts Cells TGF-β1 fibroblast myofibroblast fibrosis COVID-19 |
title | CVD and COVID-19: Emerging Roles of Cardiac Fibroblasts and Myofibroblasts |
title_full | CVD and COVID-19: Emerging Roles of Cardiac Fibroblasts and Myofibroblasts |
title_fullStr | CVD and COVID-19: Emerging Roles of Cardiac Fibroblasts and Myofibroblasts |
title_full_unstemmed | CVD and COVID-19: Emerging Roles of Cardiac Fibroblasts and Myofibroblasts |
title_short | CVD and COVID-19: Emerging Roles of Cardiac Fibroblasts and Myofibroblasts |
title_sort | cvd and covid 19 emerging roles of cardiac fibroblasts and myofibroblasts |
topic | TGF-β1 fibroblast myofibroblast fibrosis COVID-19 |
url | https://www.mdpi.com/2073-4409/11/8/1316 |
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