ArticleEMBO molecular medicine2014
FGF23 regulates renal sodium handling and blood pressure.
Article in EMBO molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06049641 (Hypertension in High School Students), which is not on this map. Cited by 183 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.
Hypertension in High School Students: Genetic and Environmental Factors
Who cites it
183 citing papers in PubMed, 314 citations in OpenAlex.
- Effects of Potassium or Sodium Supplementation on Mineral Homeostasis: A Controlled Dietary Intervention Study.The Journal of clinical endocrinology and metabolism · 2020Trial
- Response of fibroblast growth factor 23 to volume interventions in arterial hypertension and diabetic nephropathy.Medicine · 2016Trial
- Trial
- Fibroblast growth factor 23 in acute myocardial infarction complicated by cardiogenic shock: a biomarker substudy of the Intraaortic Balloon Pump in Cardiogenic Shock II (IABP-SHOCK II) trial.Critical care (London, England) · 2014Trial
- Biomaterials at the interface of bone-derived factors and inter-organ communication: Current evidence and future perspectives.Bioactive materials · 2026Review
- High-salt diet modulates endocrine regulation between cortisol and FGF23.Pflugers Archiv : European journal of physiology · 2026Article
- Fibroblast Growth Factor 23 and Outcomes in Acute Heart Failure.Biomolecules · 2026Article
- Klotho in the kidney distal convolution regulates urinary Klotho excretion and kidney calcium reabsorption, but not phosphate homeostasis.Kidney international · 2026Article
- Endocrine crosstalk in cardiovascular-kidney-metabolic syndrome-related heart failure: the fibroblast growth factor 23-Klotho axis and cardiometabolic therapy.Frontiers in endocrinology · 2026Review
- Heart Failure but Not Myocardial Infarction Is Causing Bone Loss in Rodent Models in an FGF23-Independent Manner.International journal of molecular sciences · 2025Article
- Review
- Effects of Fibroblast Growth Factor 23 (FGF23) on the Cardiovascular System: A Review of Literature.Cureus · 2025Review
- Deletion of cardiac fibroblast growth factor-23 beneficially impacts myocardial energy metabolism in left ventricular hypertrophy.npj metabolic health and disease · 2025Article
- High Dietary Phosphate Intake Induces Hypertension and Sympathetic Overactivation via Central Fibroblast Growth Factor Receptor Signaling.Circulation · 2025Article
- Genetic deletion of the sodium phosphate cotransporter NaPi2a ameliorates heart failure in mice.Scientific reports · 2025Article
- Klotho Is Cardioprotective in the mdx Mouse Model of Duchenne Muscular Dystrophy.The American journal of pathology · 2025Article
- FGF-based drug discovery: advances and challenges.Nature reviews. Drug discovery · 2025Review
- Bone-derived factors mediate crosstalk between skeletal and extra-skeletal organs.Bone research · 2025Review
- Office Blood Pressure and Obesity in Children with X-Linked Hypophosphatemia.Calcified tissue international · 2025Observational
- iFGF23 Plasma Levels in Transfusion-Dependent β-Thalassemia: Insights into Bone and Iron Metabolism.Journal of clinical medicine · 2025Article
123 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
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Fibroblast growth factor-23 (FGF23) is a bone-derived hormone regulating renal phosphate reabsorption and vitamin D synthesis in renal proximal tubules. Here, we show that FGF23 directly regulates the membrane abundance of the Na(+):Cl(-) co-transporter NCC in distal renal tubules by a signaling mechanism involving the FGF receptor/αKlotho complex, extracellular signal-regulated kinase 1/2 (ERK1/2), serum/glucocorticoid-regulated kinase 1 (SGK1), and with-no lysine kinase-4 (WNK4). Renal sodium (Na(+)) reabsorption and distal tubular membrane expression of NCC are reduced in mouse models of Fgf23 and αKlotho deficiency. Conversely, gain of FGF23 function by injection of wild-type mice with recombinant FGF23 or by elevated circulating levels of endogenous Fgf23 in Hyp mice increases distal tubular Na(+) uptake and membrane abundance of NCC, leading to volume expansion, hypertension, and heart hypertrophy in a αKlotho and dietary Na(+)-dependent fashion. The NCC inhibitor chlorothiazide abrogates FGF23-induced volume expansion and heart hypertrophy. Our findings suggest that FGF23 is a key regulator of renal Na(+) reabsorption and plasma volume, and may explain the association of FGF23 with cardiovascular risk in chronic kidney disease patients.
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What OpenQuestion holds
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.