ArticleOncotarget2016
FGF23 promotes myocardial fibrosis in mice through activation of β-catenin.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
76 citing papers in PubMed.
- Trial
- Multi-proteomic approach to predict specific cardiovascular events in patients with diabetes and myocardial infarction: findings from the EXAMINE trial.Clinical research in cardiology : official journal of the German Cardiac Society · 2021Trial
- Chronic kidney disease-associated cardiomyopathy: clinical features, pathophysiology and treatment.Nature reviews. Cardiology · 2026Review
- Three-Phase Serum Concentration Kinetics of FGF23 in a Clinical Model of Acute Myocardial Infarction.Cells · 2026Article
- Review
- Deletion of cardiac fibroblast growth factor-23 beneficially impacts myocardial energy metabolism in left ventricular hypertrophy.npj metabolic health and disease · 2025Article
- Arrhythmic burden of long-term postsurgical hypoparathyroidism assessed with 24-hour Holter ECG.Endocrine · 2025Article
- Klotho Is Cardioprotective in the mdx Mouse Model of Duchenne Muscular Dystrophy.The American journal of pathology · 2025Article
- Association of Fibroblast Growth Factor 23 and Cardiac Mechanics in the Cardiovascular Health Study.Kidney360 · 2025Article
- The mechanism by which FGF23/FGFR-1 activates NOX2-ROS in vascular endothelial cells in the context of severe heat stroke-induced acute lung injury.Burns & trauma · 2025Article
- Vitamin D-Parathyroid Hormone-Fibroblast Growth Factor 23 Axis and Cardiac Remodeling.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2025Review
- FGFR4 Is Required for Concentric Growth of Cardiac Myocytes during Physiologic Cardiac Hypertrophy.Journal of cardiovascular development and disease · 2024Article
- Non-Classical Effects of FGF23: Molecular and Clinical Features.International journal of molecular sciences · 2024Review
- Cardiac and Renal Fibrosis, the Silent Killer in the Cardiovascular Continuum: An Up-to-Date.Journal of cardiovascular development and disease · 2024Review
- Fibroblast growth factor 23 as a biomarker of right ventricular dysfunction in pulmonary hypertension.Clinical research in cardiology : official journal of the German Cardiac Society · 2023Observational
- FGF-23 is a biomarker of RV dysfunction and congestion in patients with HFrEF.Scientific reports · 2023Article
- Intact fibroblast growth factor 23 in heart failure with reduced and mildly reduced ejection fraction.BMC cardiovascular disorders · 2023Article
- Pregnancy-induced physiological hypertrophic preconditioning attenuates pathological myocardial hypertrophy by activation of FoxO3a.Cellular and molecular life sciences : CMLS · 2023Article
- Article
- Plasma FGF23 is associated with left atrial remodeling in children on hemodialysis.Pediatric nephrology (Berlin, Germany) · 2023Article
16 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibroblast growth factor 23 (FGF23) has been reported to induce left ventricular hypertrophy, but it remains unclear whether FGF23 plays a role in cardiac fibrosis. This study is attempted to investigate the role of FGF23 in post-infarct myocardial fibrosis in mice. We noted that myocardial and plasma FGF23 and FGF receptor 4 were increased in mice with heart failure as well as in cultured adult mouse cardiac fibroblasts (AMCFs) exposed to angiotensin II, phenylephrine, soluble fractalkine. Recombinant FGF23 protein increased active β-catenin , procollagen I and procollagen III expression in cultured AMCFs. Furthermore, intra-myocardial injection of adeno-associated virus-FGF23 in mice significantly increased left ventricular end-diastolic pressure and myocardial fibrosis, and markedly upregulated active β-catenin, transforming growth factor β (TGF-β), procollagen I and procollagen III in both myocardial infarction (MI) and ischemia/reperfusion (IR) mice, while β-catenin inhibitor or silencing of β-catenin antagonized the FGF23-promoted myocardial fibrosis in vitro and in vivo. These findings indicate that FGF23 promotes myocardial fibrosis and exacerbates diastolic dysfunction induced by MI or IR, which is associated with the upregulation of active β-catenin and TGF-β.
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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.