ArticleThe American journal of pathology2007
Fibroblast growth factor-2 regulates myocardial infarct repair: effects on cell proliferation, scar contraction, and ventricular function.
Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
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Who cites it
91 citing papers in PubMed, 171 citations in OpenAlex.
- Fibroblast growth factor 2 is required for epithelial recovery, but not for pulmonary fibrosis, in response to bleomycin.American journal of respiratory cell and molecular biology · 2015Trial
- Identification and characterization of a Fibrillin-1 derived matrikine for cardiac regeneration and repair.Biomaterials · 2026Article
- Translational biology of human cardiac fibrosis.Nature cardiovascular research · 2026Review
- CALIPERS: Cell cycle-aware live imaging for phenotyping experiments and regeneration studies.Nature communications · 2026Article
- Effects of epigallocatechin-3-gallate on left ventricular remodeling and functional recovery following aortic coarctation surgery.BMC cardiovascular disorders · 2026Article
- Identification and characterization of a Fibrillin-1 derived matrikine for cardiac regeneration and repair.bioRxiv : the preprint server for biology · 2025Article
- Angiogenesis: Biological Mechanisms and In Vitro Models.Annals of biomedical engineering · 2025Review
- Post-myocardial Infarction Cardiac Remodeling: Multidimensional Mechanisms and Clinical Prospects of Stem Cell Therapy.Stem cell reviews and reports · 2025Review
- Microparticle Mediated Delivery of Apelin Improves Heart Function in Post Myocardial Infarction Mice.Circulation research · 2024Article
- Repair of the Infarcted Heart: Cellular Effectors, Molecular Mechanisms and Therapeutic Opportunities.Circulation research · 2024Review
- Serum fibroblast growth factor-2 levels complement vital biomarkers for diagnosing heart failure.BMC cardiovascular disorders · 2024Article
- The involvement of soluble epoxide hydrolase in the development of cardiovascular diseases through epoxyeicosatrienoic acids.Frontiers in pharmacology · 2024Review
- Cyclical endometrial repair and regeneration: Molecular mechanisms, diseases, and therapeutic interventions.MedComm · 2023Review
- New Insights into the Reparative Angiogenesis after Myocardial Infarction.International journal of molecular sciences · 2023Review
- A single-cell comparison of adult and fetal human epicardium defines the age-associated changes in epicardial activity.Nature cardiovascular research · 2022Article
- Research Advances of Injectable Functional Hydrogel Materials in the Treatment of Myocardial Infarction.Gels (Basel, Switzerland) · 2022Review
- Intracellular Signaling Pathways Mediating Tyrosine Kinase Inhibitor Cardiotoxicity.Heart failure clinics · 2022Review
- Review
- Fibroblast growth factor receptor signaling in cardiomyocytes is protective in the acute phase following ischemia-reperfusion injury.Frontiers in cardiovascular medicine · 2022Article
- Red Blood Cell Membrane-Camouflaged PLGA Nanoparticles Loaded With Basic Fibroblast Growth Factor for Attenuating Sepsis-Induced Cardiac Injury.Frontiers in pharmacology · 2022Article
31 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Fibroblast growth factor-2 (FGF2, bFGF) has been proposed to regulate wound healing and angiogenesis, but skin wound healing in FGF2-knockout (FGF2-KO) animals is only slightly delayed. To determine the role of FGF2 in myocardial infarct repair, we studied the evolution of left ventricular geometry, cell proliferation, matrix content, and cardiac function in mice lacking or overexpressing (FGF2-Tg) FGF2. Despite having no effect on initial infarct size, deletion of FGF2 resulted in reduced fibroblast proliferation and interstitial collagen deposition, decreased endothelial proliferation and vascular density, and decreased cardiomyocyte hypertrophy. Furthermore, FGF2-KO mice demonstrated a complete absence of scar contraction, resulting in increased final infarct size and marked increases in chamber size and infarct expansion. These deficits ultimately impaired left ventricular dP/dt compared with wild-type infarcted mice. Conversely, overexpression of FGF2 increased fibroblast proliferation and collagen deposition, accelerated endothelial proliferation, and enhanced cardiomyocyte hypertrophy after infarction. These changes curbed infarct expansion and preserved left ventricular function. Thus, FGF2 is an important regulator of cell proliferation, angiogenesis, collagen synthesis, myocyte hypertrophy, scar contraction, and, ultimately, left ventricular contractile function during infarct repair. FGF2 may be more important in healing of infarcts compared with skin wounds because of the mechanical stress under which infarcts heal.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.