ArticleAmerican journal of physiology. Renal physiology2009
FGF23 decreases renal NaPi-2a and NaPi-2c expression and induces hypophosphatemia in vivo predominantly via FGF receptor 1.
Article in American journal of physiology. Renal physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 216 papers.
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Who cites it
216 citing papers in PubMed, 423 citations in OpenAlex.
- Phase II Study of BGJ398 in Patients With FGFR-Altered Advanced Cholangiocarcinoma.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2018Trial
- Pharmacokinetics and pharmacodynamics of a human monoclonal anti-FGF23 antibody (KRN23) in the first multiple ascending-dose trial treating adults with X-linked hypophosphatemia.Journal of clinical pharmacology · 2016Trial
- Impact of fractional phosphate excretion on the relation of FGF23 with outcome in CKD patients.Journal of nephrology · 2015Trial
- Prolonged Correction of Serum Phosphorus in Adults With X-Linked Hypophosphatemia Using Monthly Doses of KRN23.The Journal of clinical endocrinology and metabolism · 2015Trial
- Randomized trial of the anti-FGF23 antibody KRN23 in X-linked hypophosphatemia.The Journal of clinical investigation · 2014Trial
- Biomaterials at the interface of bone-derived factors and inter-organ communication: Current evidence and future perspectives.Bioactive materials · 2026Review
- BoneJBMR plus · 2026Article
- Bone Mineral Density Loss After Kidney Transplantation: Metabolic Determinants, Diagnostic Approaches, and Preventive Strategies.Kidney international reports · 2026Review
- Inhibition of FGFR signaling attenuates phosphaturia and early kidney injury in sickle cell disease mice.Biochemistry and biophysics reports · 2026Article
- Review
- Phosphate: An Anion Controlling Metabolic Functions.Nutrients · 2026Review
- Review
- Klotho revisited: tubular heterogeneity reshapes mineral metabolism, aging, and CKD.Pflugers Archiv : European journal of physiology · 2026Review
- Phosphaturia Exacerbates Tubular Injury and Cyst Formation in Polycystic Kidney Disease.Kidney360 · 2026Article
- Hypophosphatemia in Patients Receiving Intravenous Iron Supplementation for Iron-Deficiency Anemia: A Narrative Review.Journal of clinical medicine · 2026Review
- Tumor-targeted bispecific antibodies effectively inhibit oncogenic pathways while minimizing toxicity.Science advances · 2026Article
- X-linked Hypophosphatemic Rickets Revealed by Exome Sequencing: A Pediatric Case Report of a PHEX Pathogenic Variant.Cureus · 2026Article
- Fibroblast growth factor 23: Regulation, signalling and systemic links between bone, metabolism and inflammation.Molecular metabolism · 2026Review
- Klotho in the kidney distal convolution regulates urinary Klotho excretion and kidney calcium reabsorption, but not phosphate homeostasis.Kidney international · 2026Article
- Molecular Basis of Rare Inherited Tubulopathies of the Kidney: A Primer for Clinicians.International journal of molecular sciences · 2026Review
156 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
Fibroblast growth factor-23 (FGF23) is a phosphaturic hormone that contributes to several hypophosphatemic disorders by reducing the expression of the type II sodium-phosphate cotransporters (NaPi-2a and NaPi-2c) in the kidney proximal tubule and by reducing serum 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] levels. The FGF receptor(s) mediating the hypophosphatemic action of FGF23 in vivo have remained elusive. In this study, we show that proximal tubules express FGFR1, -3, and -4 but not FGFR2 mRNA. To determine which of these three FGFRs mediates FGF23's hypophosphatemic actions, we characterized phosphate homeostasis in FGFR3(-/-) and FGFR4(-/-) null mice, and in conditional FGFR1(-/-) mice, with targeted deletion of FGFR1 expression in the metanephric mesenchyme. Basal serum phosphorus levels and renal cortical brush-border membrane (BBM) NaPi-2a and NaPi-2c expression were comparable between FGFR1(-/-), FGFR3(-/-), and FGFR4(-/-) mice and their wild-type counterparts. Administration of FGF23 to FGFR3(-/-) mice induced hypophosphatemia in these mice (8.0 +/- 0.4 vs. 5.4 +/- 0.3 mg/dl; p < or = 0.001) and a decrease in renal BBM NaPi-2a and NaPi-2c protein expression. Similarly, in FGFR4(-/-) mice, administration of FGF23 caused a small but significant decrease in serum phosphorus levels (8.7 +/- 0.3 vs. 7.6 +/- 0.4 mg/dl; p < or = 0.001) and in renal BBM NaPi-2a and NaPi-2c protein abundance. In contrast, injection of FGF23 into FGFR1(-/-) mice had no effects on serum phosphorus levels (5.6 +/- 0.3 vs. 5.2 +/- 0.5 mg/dl) or BBM NaPi-2a and NaPi-2c expression. These data show that FGFR1 is the predominant receptor for the hypophosphatemic action of FGF23 in vivo, with FGFR4 likely playing a minor role.
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