ArticleExperimental cell research2013
Cardiomyocyte FGF signaling is required for Cx43 phosphorylation and cardiac gap junction maintenance.
Article in Experimental cell research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 29 citations in OpenAlex.
- Mild hypothermia (35°C) reduces myocardial ischemia-reperfusion injury and attenuates hypoxia induced apoptosis of H9C2 cardiomyocytes by changing the phosphorylation level of Connexin43 (Cx43) protein.African health sciences · 2025Article
- Post translational modifications of connexin 43 in ventricular arrhythmias after myocardial infarction.Molecular biology reports · 2024Review
- The translation initiation factor homolog eif4e1c regulates cardiomyocyte metabolism and proliferation during heart regeneration.Development (Cambridge, England) · 2023Article
- Nr2f1a maintains atrialeLife · 2023Article
- Understanding the Role of ATP Release through Connexins Hemichannels during Neurulation.International journal of molecular sciences · 2023Article
- The FGF-AKT pathway is necessary for cardiomyocyte survival for heart regeneration in zebrafish.Developmental biology · 2021Article
- hiPSC-Derived Cardiac Tissue for Disease Modeling and Drug Discovery.International journal of molecular sciences · 2020Review
- The Microenvironment of Decellularized Extracellular Matrix from Heart Failure Myocardium Alters the Balance between Angiogenic and Fibrotic Signals from Stromal Primitive Cells.International journal of molecular sciences · 2020Article
- Heritable arrhythmia syndromes associated with abnormal cardiac sodium channel function: ionic and non-ionic mechanisms.Cardiovascular research · 2020Review
- Gap junction-mediated cell-to-cell communication in oral development and oral diseases: a concise review of research progress.International journal of oral science · 2020Review
- Prevention of connexin-43 remodeling protects against Duchenne muscular dystrophy cardiomyopathy.The Journal of clinical investigation · 2020Article
- Engineering hiPSC cardiomyocyte in vitro model systems for functional and structural assessment.Progress in biophysics and molecular biology · 2019Review
- Collagen Type I Containing Hybrid Hydrogel Enhances Cardiomyocyte Maturation in a 3D Cardiac Model.Polymers · 2019Article
- Cardiotoxic Effects of Short-Term Doxorubicin Administration: Involvement of Connexin 43 in Calcium Impairment.International journal of molecular sciences · 2017Article
- Article
- Normal versus Pathological Cardiac Fibroblast-Derived Extracellular Matrix Differentially Modulates Cardiosphere-Derived Cell Paracrine Properties and Commitment.Stem cells international · 2017Article
- Neuroprotective Effect of Salvianolic Acids against Cerebral Ischemia/Reperfusion Injury.International journal of molecular sciences · 2016Article
- Mechanism of Mitochondrial Connexin43's Protection of the Neurovascular Unit under Acute Cerebral Ischemia-Reperfusion Injury.International journal of molecular sciences · 2016Article
- Fibroblast growth factors, old kids on the new block.Seminars in cell & developmental biology · 2016Review
- Dynamic changes in protein interaction between AKAP95 and Cx43 during cell cycle progression of A549 cells.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Cardiac remodeling resulting from impairment of myocardial integrity leads to heart failure, through still incompletely understood mechanisms. The fibroblast growth factor (FGF) system has been implicated in tissue maintenance, but its role in the adult heart is not well defined. We hypothesized that the FGF system plays a role in the maintenance of cardiac homeostasis, and the impairment of cardiomyocyte FGF signaling leads to pathological cardiac remodeling. We showed that FGF signaling is required for connexin 43 (Cx43) localization at cell-cell contacts in isolated cardiomyocytes and COS7 cells. Lack of FGF signaling led to decreased Cx43 phosphorylation at serines 325/328/330 (S325/328/330), sites known to be important for assembly of gap junctions. Cx43 instability induced by FGF inhibition was restored by the Cx43 S325/328/330 phospho-mimetic mutant, suggesting FGF-dependent phosphorylation of these sites. Consistent with these in vitro findings, cardiomyocyte-specific inhibition of FGF signaling in adult mice demonstrated mislocalization of Cx43 at intercalated discs, whereas localization of N-cadherin and desmoplakin was not affected. This led to premature death resulting from impaired cardiac remodeling. We conclude that cardiomyocyte FGF signaling is essential for cardiomyocyte homeostasis through phosphorylation of Cx43 at S325/328/330 residues which are important for the maintenance of gap junction.
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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.