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Updated: Jun 12, 2026

Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model
Published on: July 3, 2020
[Bone and joint diseases in children. Phosphaturic hormone, FGF23, and bone metabolism]
1Department of Pediatrics, Osaka University School of Medicine.
Insights
Fibroblast growth factor 23 (FGF23) is an endocrine factor that regulates phosphate. Elevated FGF23 causes hypophosphatemia, rickets, and osteomalacia, and is implicated in various genetic and tumor-induced hypophosphatemia forms.
Area of Science:
- Endocrinology
- Molecular Biology
- Genetics
Background:
- Fibroblast growth factor 23 (FGF23) is a key endocrine regulator of phosphate homeostasis.
- Elevated FGF23 levels are associated with hypophosphatemia, rickets, and osteomalacia.
- FGF23 plays a role in the pathogenesis of diverse hypophosphatemia types, including genetic and tumor-induced forms.
Purpose of the Study:
- To elucidate the role of FGF23 in phosphate metabolism and related bone disorders.
- To understand the involvement of FGF23 in various forms of hypophosphatemia.
- To describe the receptor complex for FGF23.
Main Methods:
- Review of existing literature on FGF23 and hypophosphatemia.
- Analysis of FGF23's phosphaturic effects.
- Description of the FGF23 receptor complex.
Main Results:
- FGF23 exhibits a phosphaturic effect, lowering serum phosphate levels.
- High FGF23 concentrations lead to hypophosphatemia, rickets, and osteomalacia.
- FGF23 is implicated in autosomal, X-linked, and tumor-induced hypophosphatemia.
Conclusions:
- FGF23 is a critical hormone in phosphate regulation and bone health.
- Dysregulation of FGF23 contributes to significant mineral and bone disorders.
- Alpha klotho and FGF receptor type 1 form the specific receptor for FGF23.
Abstract:
Fibroblast growth factor 23 (FGF23) belongs to FGF19 subfamily, whose members function like endocrine factors, and has a phosphaturic effect, leading to hypophosphatemia associated with rickets or osteomalacia when its concentration in blood is elevated. FGF23 is involved in the pathogenesis in many forms of hypophosphatemia including the autosomal dominant and recessive types, the X-linked type and the tumor-induced type. Alpha klotho, originally discovered as an anti-aging factor, along with the FGF receptor type 1 makes a specific receptor for FGF23.
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