ArticleThe Journal of biological chemistry2013
FGF23 suppresses chondrocyte proliferation in the presence of soluble α-Klotho both in vitro and in vivo.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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26 citing papers in PubMed, 55 citations in OpenAlex.
- Genome-Wide Identification of Candidate Genes Associated with Antler Weight in Tahe Red Deer.Animals : an open access journal from MDPI · 2026Article
- Experts' consensus on the management and treatment of individuals with X-linked hypophosphatemia across lifespan.Journal of endocrinological investigation · 2025Article
- Clinical practice recommendations for the diagnosis and management of X-linked hypophosphataemia.Nature reviews. Nephrology · 2025Review
- The Diagnosis and Therapy of XLH.Calcified tissue international · 2025Review
- Fibroblast Growth Factor 19 Disrupts Cartilage Development Via the FGFR4/β-catenin Axis.International journal of biological sciences · 2025Article
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- Progress of Wnt Signaling Pathway in Osteoporosis.Biomolecules · 2023Review
- Meclozine ameliorates bone mineralization and growth plate structure in a mouse model of X‑linked hypophosphatemia.Experimental and therapeutic medicine · 2023Article
- Growth hormone treatment improves final height in children with X-linked hypophosphatemia.Orphanet journal of rare diseases · 2022Article
- Klotho Ameliorates Vascular Calcification via Promoting Autophagy.Oxidative medicine and cellular longevity · 2022Article
- FGF/FGFR signaling in health and disease.Signal transduction and targeted therapy · 2020Review
- Description of a novelTherapeutic advances in musculoskeletal disease · 2020Article
- A Mutation inFrontiers in cell and developmental biology · 2020Article
- Mutant hFGF23(A12D) stimulates osteoblast differentiation through FGFR3.Journal of cellular and molecular medicine · 2019Article
- FGF23 and its role in X-linked hypophosphatemia-related morbidity.Orphanet journal of rare diseases · 2019Review
- Article
- FTO demethylase activity is essential for normal bone growth and bone mineralization in mice.Biochimica et biophysica acta. Molecular basis of disease · 2018Article
- FGF23 Actions on Target Tissues-With and Without Klotho.Frontiers in endocrinology · 2018Review
- Inhibition of FGFR Signaling Partially Rescues Hypophosphatemic Rickets in HMWFGF2 Tg Male Mice.Endocrinology · 2017Article
- The metabolic bone disease associated with theBone reports · 2017Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibroblast growth factor-23 (FGF23) is well established to play crucial roles in the regulation of phosphate homeostasis. X-linked hypophosphatemic rickets (XLH) is characterized by impaired mineralization and growth retardation associated with elevated circulating FGF23 levels. Administration of phosphate and calcitriol is effective in improving growth retardation, but is not sufficient to fully reverse impaired growth, suggesting the existence of a disease-specific mechanism in the development of growth retardation in addition to dysregulated phosphate metabolism. However, the precise mechanisms of growth retardation in XLH remain elusive. Here, we postulated that FGF23 suppressed chondrocyte proliferation in the presence of soluble α-Klotho (sKL). In vitro and ex vivo studies revealed that FGF23 formed a protein complex with sKL through KL1 internal repeat and suppressed the linear growth of metatarsals in the presence of sKL, which was antagonized by co-incubation with neutralizing antibodies against FGF23 or by knocking-down FGFR3 expression. Additionally, FGF23 binding to FGFR3 was enhanced in the presence of sKL. Histologically, the length of the proliferating zone was diminished and was associated with decreased chondrocyte proliferation. FGF23/sKL suppressed Indian hedgehog (Ihh) expression and administration of Ihh protein partially rescued the suppressive effect of FGF23/sKL on metatarsal growth. Intraperitoneal administration of sKL in Hyp mice, a murine model for XLH, caused a decrease in the length of the proliferating zone associated with decreased chondrocyte proliferation without altering circulating phosphate levels. These findings suggest that suppression of chondrocyte proliferation by FGF23 could have a causative role in the development of growth retardation in XLH.
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