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Cardiac Fibrosis: The Fibroblast Awakens
Open accessAbstract
Myocardial fibrosis is a significant global health problem associated with nearly all forms of heart disease. Cardiac fibroblasts comprise an essential cell type in the heart that is responsible for the homeostasis of the extracellular matrix; however, upon injury, these cells transform to a myofibroblast phenotype and contribute to cardiac fibrosis. This remodeling involves pathological changes that include chamber dilation, cardiomyocyte hypertrophy and apoptosis, and ultimately leads to the progression to heart failure. Despite the critical importance of fibrosis in cardiovascular disease, our limited understanding of the cardiac fibroblast impedes the development of potential therapies that effectively target this cell type and its pathological contribution to disease progression. This review summarizes current knowledge regarding the origins and roles of fibroblasts, mediators and signaling pathways known to influence fibroblast function after myocardial injury, as well as novel therapeutic strategies under investigation to attenuate cardiac fibrosis.
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“Nearly all cardiac diseases involve pathological fibrotic remodeling caused by CF proliferation and ECM deposition53.”
From 3D bioprinting of high cell-density heterogeneous tissue models through spheroid fusion within self-healing hydrogels (2021) · cites this paper as [53]
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“Focal cardiac fibrosis that arises post-MI is a major clinical burden that often leads to a cascade of pathological remodeling and may result in heart failure53.”
From 3D bioprinting of high cell-density heterogeneous tissue models through spheroid fusion within self-healing hydrogels (2021) · cites this paper as [53]
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“CFs themselves cannot generate action potentials”
From 3D bioprinting of high cell-density heterogeneous tissue models through spheroid fusion within self-healing hydrogels (2021) · cites this paper as [53]
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“excessive ECM production reduces cardiomyocyte-cardiomyocyte (CM) connectivity, leading to reduced tissue compliance and electrical synchronization53.”
From 3D bioprinting of high cell-density heterogeneous tissue models through spheroid fusion within self-healing hydrogels (2021) · cites this paper as [53]
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Metadata
- Authors
- Travers, J. G., Kamal, F. A., Robbins, J., Yutzey, K. E., & Blaxall, B. C.
- Affiliations
- Cincinnati Children's Hospital Medical Center (US)
- Venue
- Circulation Research
- Published
- 2016-03-18
- Volume
- 118
- Issue
- 6
- Pages
- 1021-1040
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- PMC
- PMC4800485
- OpenAlex
- W2299099463
- Cited by
- 1,596
- References
- 261
- Citations by year
- 2026: 156 · 2025: 175 · 2024: 184 · 2023: 182 · 2022: 156 · 2021: 211 · 2020: 163 · 2019: 143 · 2018: 98 · 2017: 95 · 2016: 30
- FWCI
- 21.30
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Circulation Research (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (P01HL069779, R01HL129772, R01HL091475, R01HL134312, R01HL132551, R01HL133695, U54HL119810)
- National Institute of General Medical Sciences (R01GM097347)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Keywords
- myocardial fibrosis, cardiac fibroblasts, myofibroblast differentiation, extracellular matrix homeostasis, myocardial injury, cardiac remodeling, cardiomyocyte hypertrophy, cardiomyocyte apoptosis, heart failure, signaling pathways, treatment options
- MeSH terms
- Animals, Fibroblasts, Fibrosis, Heart Failure, Humans, Cardiomyopathies, Inflammation Mediators, Myofibroblasts
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