Cardiac Fibrosis: The Fibroblast Awakens

Travers, Joshua G.; Kamal, Fadia A.; Robbins, Jeffrey; Yutzey, Katherine E.; Blaxall, Burns C.

doi:10.1161/circresaha.115.306565

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

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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Nearly all cardiac diseases involve pathological fibrotic remodeling caused by CF proliferation and ECM deposition.
“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]
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 failure.
“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]
Cardiac fibroblasts cannot generate action potentials.
“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]
Excessive ECM production reduces cardiomyocyte-cardiomyocyte connectivity, leading to reduced tissue compliance and electrical synchronization.
“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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Origin, development, and differentiation of cardiac fibroblasts
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Targeted inhibition of activin receptor-like kinase 5 signaling attenuates cardiac dysfunction following myocardial infarction
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Angiotensin-Converting Enzyme Inhibition and Ventricular Remodeling After Myocardial Infarction
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Progenitor Cells Identified by PDGFR-Alpha Expression in the Developing and Diseased Human Heart
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Cerebral microvascular pericytes and neurogliovascular signaling in health and disease
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Systematic Characterization of Myocardial Inflammation, Repair, and Remodeling in a Mouse Model of Reperfused Myocardial Infarction
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IL-1β stimulates rat cardiac fibroblast migration via MAP kinase pathways
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G Protein Coupled Receptor Kinases as Therapeutic Targets in Cardiovascular Disease
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Self-citation
IL-6 loss causes ventricular dysfunction, fibrosis, reduced capillary density, and dramatically alters the cell populations of the developing and adult heart
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C-Reactive Protein Promotes Cardiac Fibrosis and Inflammation in Angiotensin II–Induced Hypertensive Cardiac Disease
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Interactions between cardiac cells enhance cardiomyocyte hypertrophy and increase fibroblast proliferation
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Pressure Overload-Induced Transient Oxidative Stress Mediates Perivascular Inflammation and Cardiac Fibrosis through Angiotensin II
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The role of angiotensin II, endothelin-1 and transforming growth factor-β as autocrine/paracrine mediators of stretch-induced cardiomyocyte hypertrophy
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Angiotensin II increases collagen I expression via transforming growth factor-beta1 and extracellular signal-regulated kinase in cardiac fibroblasts
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The Alveolar Epithelium Determines Susceptibility to Lung Fibrosis in Hermansky-Pudlak Syndrome
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Identification and characterization of a novel Schwann and outflow tract endocardial cushion lineage-restricted periostin enhancer
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Electrophysiological Modeling of Fibroblasts and their Interaction with Myocytes
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Characterization of Pdgfrb‐Cre transgenic mice reveals reduction of ROSA26 reporter activity in remodeling arteries
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Transforming Growth Factor β1 Induces αvβ3 Integrin Expression in Human Lung Fibroblasts via a β3 Integrin-, c-Src-, and p38 MAPK-dependent Pathway
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Reciprocal Interaction between Macrophages and T cells Stimulates IFN-γ and MCP-1 Production in Ang II-induced Cardiac Inflammation and Fibrosis
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Platelet-derived growth factor-D promotes fibrogenesis of cardiac fibroblasts
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Self-citation
Heart-Infiltrating Prominin-1 + /CD133 + Progenitor Cells Represent the Cellular Source of Transforming Growth Factor β–Mediated Cardiac Fibrosis in Experimental Autoimmune Myocarditis
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Connective Tissue Growth Factor Inhibition Attenuates Left Ventricular Remodeling and Dysfunction in Pressure Overload–Induced Heart Failure
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Platelet‐derived growth factor receptor‐α cells in mouse urinary bladder: a new class of interstitial cells
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ET-1 from endothelial cells is required for complete angiotensin II-induced cardiac fibrosis and hypertrophy
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Identification of Direct Serum-response Factor Gene Targets during Me2SO-induced P19 Cardiac Cell Differentiation
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3 of the 261 references couldn’t be matched to a known paper.

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Angiotensin II Signal Transduction: An Update on Mechanisms of Physiology and Pathophysiology
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Cardiorenal Syndrome Revisited
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The Role of Oxidative Stress in Myocardial Ischemia and Reperfusion Injury and Remodeling: Revisited
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Metabolic mechanisms in physiological and pathological cardiac hypertrophy: new paradigms and challenges
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Self-Healing Hydrogels: Preparation, Mechanism and Advancement in Biomedical Applications
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The epicardium as a hub for heart regeneration
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Th1 effector T cells selectively orchestrate cardiac fibrosis in nonischemic heart failure
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Bearing My Heart: The Role of Extracellular Matrix on Cardiac Development, Homeostasis, and Injury Response
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Mechanical regulation of gene expression in cardiac myocytes and fibroblasts
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Cardiac Fibroblast Activation Post-Myocardial Infarction: Current Knowledge Gaps
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Loss of β-catenin in resident cardiac fibroblasts attenuates fibrosis induced by pressure overload in mice
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Self-citation
CNS fibroblasts form a fibrotic scar in response to immune cell infiltration.
Dorrier, C. E., Aran, D., Haenelt, E. A., Sheehy, R. N., Hoi, K. K., Pintarić, L., Chen, Y., Lizama, C. O., Cautivo, K. M., Weiner, G. A., et al. (2021) · Nature Neuroscience · doi:10.1038/s41593-020-00770-9 · Cited by 199 · see citing works
Cardiac fibrosis: potential therapeutic targets
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Therapeutic approaches to control tissue repair and fibrosis: Extracellular matrix as a game changer
Walraven, M., & Hinz, B. (2018) · Matrix Biology · doi:10.1016/j.matbio.2018.02.020 · Cited by 194 · see citing works
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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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Cardiac Fibrosis: The Fibroblast Awakens

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