ArticleiScience2020
FGF13 Is a Novel Regulator of NF-κB and Potentiates Pathological Cardiac Hypertrophy.
Article in iScience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- Fibroblast growth factor 13 deficiency attenuates doxorubicin-induced cardiotoxicity by regulating Parkin-mediated myocardial injury.Acta biochimica et biophysica Sinica · 2026Article
- Inhibition of Neuroinflammation by Costunolide Attenuates Hypoxic-Ischemic Brain Damage via the PI3K/AKT Pathway in Neonatal Rats.Molecular neurobiology · 2025Article
- An infusible decellularized extracellular matrix material binds to vasculature in infarcted myocardium and induces pro-reparative gene expression following acute myocardial infarction through inherent avidity and bioactive signaling.bioRxiv : the preprint server for biology · 2025Article
- Effects of open-channel blocking peptides in NaBiophysical journal · 2025Article
- The FGF13-Caveolin-1 Axis: A Key Player in the Pathogenesis of Doxorubicin- and D-Galactose-Induced Premature Cardiac Aging.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The Abl1 tyrosine kinase is a key player in doxorubicin-induced cardiomyopathy and its p53/p73 cell death mediated signaling differs in atrial and ventricular cardiomyocytes.Journal of translational medicine · 2024Article
- Article
- InducibleActa biochimica et biophysica Sinica · 2024Article
- Reduced expression of transmembrane protein 43 during cardiac hypertrophy leads to worsening heart failure in mice.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- NF-κB, A Potential Therapeutic Target in Cardiovascular Diseases.Cardiovascular drugs and therapy · 2023Review
- Fibroblast growth factor 18 alleviates stress-induced pathological cardiac hypertrophy in male mice.Nature communications · 2023Article
- FGF12 is a novel component of the nucleolar NOLC1/TCOF1 ribosome biogenesis complex.Cell communication and signaling : CCS · 2022Article
- Lupeol protects against cardiac hypertrophy via TLR4-PI3K-Akt-NF-κB pathways.Acta pharmacologica Sinica · 2022Article
- New developments in the biology of fibroblast growth factors.WIREs mechanisms of disease · 2022Review
- Fibroblast growth factor homologous factors serve as a molecular rheostat in tuning arrhythmogenic cardiac late sodium current.Nature cardiovascular research · 2022Article
- Fibroblast growth factor 20 attenuates pathological cardiac hypertrophy by activating the SIRT1 signaling pathway.Cell death & disease · 2022Article
- Review
- The Multifunctional Contribution of FGF Signaling to Cardiac Development, Homeostasis, Disease and Repair.Frontiers in cell and developmental biology · 2021Review
- Fibroblast Growth Factor (FGF) 13.Differentiation; research in biological diversityReview
Corrections and comments
- Erratum issued
Authors and funding
16 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FGF13 is an intracellular FGF factor. Its role in cardiomyopathies has been rarely investigated. We revealed that endogenous FGF13 is up-regulated in cardiac hypertrophy accompanied by increased nuclear localization. The upregulation of FGF13 plays a deteriorating role both in hypertrophic cardiomyocytes and mouse hearts. Mechanistically, FGF13 directly interacts with p65 by its nuclear localization sequence and co-localizes with p65 in the nucleus in cardiac hypertrophy. FGF13 deficiency inhibits NF-κB activation in ISO-treated NRCMs and TAC-surgery mouse hearts, whereas FGF13 overexpression shows the opposite trend. Moreover, FGF13 overexpression alone is sufficient to activate NF-κB in cardiomyocytes. The interaction between FGF13 and p65 or the effects of FGF13 on NF-κB have nothing to do with IκB. Together, an IκB-independent mechanism for NF-κB regulation has been revealed in cardiomyocytes both under basal and stressful conditions, suggesting the promising application of FGF13 as a therapeutic target for pathological cardiac hypertrophy and heart failure.
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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.