ArticleAmerican journal of physiology. Endocrinology and metabolism2013
FGF23 is a novel regulator of intracellular calcium and cardiac contractility in addition to cardiac hypertrophy.
Article in American journal of physiology. Endocrinology and metabolism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers.
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Who cites it
124 citing papers in PubMed, 194 citations in OpenAlex.
- A Low-Sodium DASH Dietary Pattern Affects Serum Markers of Inflammation and Mineral Metabolism in Adults with Elevated Blood Pressure.The Journal of nutrition · 2021Trial
- Association of Fibroblast Growth Factor 23 With Recurrent Cardiovascular Events in Patients After an Acute Coronary Syndrome: A Secondary Analysis of a Randomized Clinical Trial.JAMA cardiology · 2018Trial
- Trial
- Fibroblast growth factor-23, cardiovascular prognosis, and benefit of angiotensin-converting enzyme inhibition in stable ischemic heart disease.Journal of the American College of Cardiology · 2014Trial
- FGF23 promotes atrial fibrillation susceptibility through ETV1-dependent sodium channel regulation and calcium handling abnormalities.Experimental physiology · 2026Article
- The Binding of Fibroblast Growth Factor 23 (FGF23) to FGF Receptor-αKlotho Complex Increases Sinoatrial Electrical Activity.Acta physiologica (Oxford, England) · 2026Article
- Fibroblast growth factor 23: Regulation, signalling and systemic links between bone, metabolism and inflammation.Molecular metabolism · 2026Review
- X-Linked Hypophosphatemia: Role of Fibroblast Growth Factor 23 on Human Skeletal Muscle-Derived Cells.Calcified tissue international · 2025Article
- Mechanisms underlying atrial fibrillation in chronic kidney disease.Journal of molecular and cellular cardiology · 2025Review
- Bone mechanical loading reduces heart rate and increases heart rate variability in mice.Bone reports · 2025Article
- MLO-Y4 fluid flow shear stress conditioned media enhances cardiac contractility and intracellular CaAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2025Article
- Klotho Is Cardioprotective in the mdx Mouse Model of Duchenne Muscular Dystrophy.The American journal of pathology · 2025Article
- Cardiac FGF23 Increases Intracellular Calcium in Atrial Myocytes and the Susceptibility to Atrial Fibrillation Decreased in FGF23Journal of cellular and molecular medicine · 2025Article
- Heart Failure and Osteoporosis: Shared Challenges in the Aging Population.Journal of cardiovascular development and disease · 2025Review
- Baseline fibroblast growth factor 23 predicts incident heart failure and cardiovascular mortality in patients with chronic kidney disease: A 3-year follow-up study.International journal of cardiology. Heart & vasculature · 2025Article
- Vitamin D-Parathyroid Hormone-Fibroblast Growth Factor 23 Axis and Cardiac Remodeling.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2025Review
- Enhancing gene transfer to renal tubules and podocytes by context-dependent selection of AAV capsids.Nature communications · 2024Article
- Non-Classical Effects of FGF23: Molecular and Clinical Features.International journal of molecular sciences · 2024Review
- Phosphate in Cardiovascular Disease: From New Insights Into Molecular Mechanisms to Clinical Implications.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- FGF23 and klotho at the intersection of kidney and cardiovascular disease.Nature reviews. Cardiology · 2024Review
64 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
Fibroblast growth factor 23 (FGF23) is a hormone released primarily by osteocytes that regulates phosphate and vitamin D metabolism. Recent observational studies in humans suggest that circulating FGF23 is independently associated with cardiac hypertrophy and increased mortality, but it is unknown whether FGF23 can directly alter cardiac function. We found that FGF23 significantly increased cardiomyocyte cell size in vitro, the expression of gene markers of cardiac hypertrophy, and total protein content of cardiac muscle. In addition, FGFR1 and FGFR3 mRNA were the most abundantly expressed FGF receptors in cardiomyocytes, and the coreceptor α-klotho was expressed at very low levels. We tested an animal model of chronic kidney disease (Col4a3(-/-) mice) that has elevated serum FGF23. We found elevations in common hypertrophy gene markers in Col4a3(-/-) hearts compared with wild type but did not observe changes in wall thickness or cell size by week 10. However, the Col4a3(-/-) hearts did show reduced fractional shortening (-17%) and ejection fraction (-11%). Acute exposure of primary cardiomyocytes to FGF23 resulted in elevated intracellular Ca(2+) ([Ca(2+)](i); F/F(o) + 86%) which was blocked by verapamil pretreatment. FGF23 also increased ventricular muscle strip contractility (67%), which was inhibited by FGF receptor antagonism. We hypothesize that although FGF23 can acutely increase [Ca(2+)](i), chronically this may lead to decreases in contractile function or stimulate cardiac hypertrophy, as observed with other stress hormones. In conclusion, FGF23 is a novel bone/heart endocrine factor and may be an important mediator of cardiac Ca(2+) regulation and contractile function during chronic kidney disease.
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