ArticlePloS one2013
Fibroblast growth factor receptor 1 signaling in adult cardiomyocytes increases contractility and results in a hypertrophic cardiomyopathy.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 48 citations in OpenAlex.
- Activating FGFR1 restores Integrin-β1-mediated fibronectin sensing in satellite cells of aged mice.bioRxiv : the preprint server for biology · 2026Article
- Integrative Transcriptomic-Histological Analysis in Dilated Cardiomyopathy Unveils FGFR1 Inhibition as Anti-Cardiac Fibrotic and Cardioprotective Therapy.JACC. Basic to translational science · 2025Article
- Cardiac Fibroblasts: Helping or Hurting.Genes · 2025Review
- Cell cycle arrest of cardiomyocytes in the context of cardiac regeneration.Frontiers in cardiovascular medicine · 2025Review
- Identification of Circulating Plasma Proteins as a Mediator of Hypertension-Driven Cardiac Remodeling: A Mediation Mendelian Randomization Study.Hypertension (Dallas, Tex. : 1979) · 2024Article
- Hyperglycemia activates FGFR1Acta pharmaceutica Sinica. B · 2024Article
- Intact fibroblast growth factor 23 in heart failure with reduced and mildly reduced ejection fraction.BMC cardiovascular disorders · 2023Article
- Characterization of a robust mouse model of heart failure with preserved ejection fraction.American journal of physiology. Heart and circulatory physiology · 2023Article
- New developments in the biology of fibroblast growth factors.WIREs mechanisms of disease · 2022Review
- Intracellular Signaling Pathways Mediating Tyrosine Kinase Inhibitor Cardiotoxicity.Heart failure clinics · 2022Review
- A Bioinformatic Approach Based on Systems Biology to Determine the Effects of SARS-CoV-2 Infection in Patients with Hypertrophic Cardiomyopathy.Computational and mathematical methods in medicine · 2022Article
- Fibroblast growth factor receptor signaling in cardiomyocytes is protective in the acute phase following ischemia-reperfusion injury.Frontiers in cardiovascular medicine · 2022Article
- Endothelial FGF signaling is protective in hypoxia-induced pulmonary hypertension.The Journal of clinical investigation · 2021Article
- Upregulation of interleukin-8 and activin A induces osteoclastogenesis in ameloblastoma.International journal of molecular medicine · 2019Article
- ERK: A Key Player in the Pathophysiology of Cardiac Hypertrophy.International journal of molecular sciences · 2019Review
- The Impact of Pazopanib on the Cardiovascular System.Journal of cardiovascular pharmacology and therapeutics · 2018Review
- Klotho is upregulated in human cardiomyopathy independently of circulating Klotho levels.Scientific reports · 2018Article
- Calcitriol downregulates fibroblast growth factor receptor 1 through histone deacetylase activation in HL-1 atrial myocytes.Journal of biomedical science · 2018Article
- Increased Circulating FGF23 Does Not Lead to Cardiac Hypertrophy in the Male Hyp Mouse Model of XLH.Endocrinology · 2018Article
- Review
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Fibroblast growth factors (FGFs) and their receptors are highly conserved signaling molecules that have been implicated in postnatal cardiac remodeling. However, it is not known whether cardiomyocyte-expressed FGF receptors are necessary or sufficient for ventricular remodeling in the adult heart. To determine whether cardiomyocytes were competent to respond to an activated FGF receptor, and to determine if this signal would result in the development of hypertrophy, we engineered a doxycycline (DOX)-inducible, cardiomyocyte-specific, constitutively active FGF receptor mouse model (αMHC-rtTA, TRE-caFgfr1-myc). Echocardiographic and hemodynamic analysis indicated that acute expression of caFGFR1 rapidly and directly increased cardiac contractility, while chronic expression resulted in significant hypertrophy with preservation of systolic function. Subsequent histologic analysis showed increased cardiomyocyte cross-sectional area and regions of myocyte disarray and fibrosis, classic features of hypertrophic cardiomyopathy (HCM). Analysis of downstream pathways revealed a lack of clear activation of classical FGF-mediated signaling pathways, but did demonstrate a reduction in Serca2 expression and troponin I phosphorylation. Isolated ventricular myocytes showed enhanced contractility and reduced relaxation, an effect that was partially reversed by inhibition of actin-myosin interactions. We conclude that adult cardiomyocytes are competent to transduce FGF signaling and that FGF signaling is sufficient to promote increased cardiomyocyte contractility in vitro and in vivo through enhanced intrinsic actin-myosin interactions. Long-term, FGFR overexpression results in HCM with a dynamic outflow tract obstruction, and may serve as a unique model of HCM.
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