Cited by 1,596Cardiac Fibrosis and RemodelingCongenital heart defects researchLiver physiology and pathology

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Cardiac Fibrosis: The Fibroblast Awakens

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Travers, Joshua G., Kamal, Fadia A., Robbins, Jeffrey, Yutzey, Katherine E., Blaxall, Burns C.·2016·Circulation Research

DOI 10.1161/circresaha.115.306565PMC PMC4800485

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Abstract

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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Authors: Travers, J. G., Kamal, F. A., Robbins, J., Yutzey, K. E., & Blaxall, B. C.
Affiliations: Cincinnati Children's Hospital Medical Center (US)
ORCID: Travers, Joshua G.
Kamal, Fadia A.
Robbins, Jeffrey
Yutzey, Katherine E.
Venue: Circulation Research
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 2016-03-18
Volume: 118
Issue: 6
Pages: 1021-1040
ISSN: 0009-7330 (ISSN-L)
1524-4571
DOI: 10.1161/circresaha.115.306565
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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