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Article

Homozygous ablation of fibroblast growth factor-23 results in hyperphosphatemia and impaired skeletogenesis, and reverses hypophosphatemia in Phex-deficient mice.

Matrix biology : journal of the International Society for Matrix Biology - 1 Nov 2004

Sitara Despina, Razzaque Mohammed S, Hesse Martina, Yoganathan Subbiah, Taguchi Takashi, Erben Reinhold G, Jüppner Harald, Lanske Beate

Abstract excerpt

Fibroblast growth factor-23 (FGF-23), a recently identified molecule that is mutated in patients with autosomal dominant hypophosphatemic rickets (ADHR), appears to be involved in the regulation of phosphate homeostasis. Although increased levels of circulating FGF-23 were detected in patients with different phosphate-wasting disorders such as oncogenic osteomalacia (OOM) and X-linked hypophosphatemia (XLH), it...

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Identifiers

PMID: 15579309
DOI: 10.1016/j.matbio.2004.09.007
PMCID: PMC2894977

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Homozygous ablation of fibroblast growth factor-23 results in hyperphosphatemia and impaired skeletogenesis, and reverses hypophosphatemia in Phex-deficient mice.PMID 15579309Read ↗

Transgenic mice expressing fibroblast growth factor 23 under the control of the alpha1(I) collagen promoter exhibit growth retardation, osteomalacia, and disturbed phosphate homeostasis.Semantic proximity Read ↗

FGF23 and its role in X-linked hypophosphatemia-related morbiditySemantic proximity Read ↗

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Overexpression of the DMP1 C-terminal fragment stimulates FGF23 and exacerbates the hypophosphatemic rickets phenotype in Hyp mice.Semantic proximity Read ↗

A Phex mutation in a murine model of X-linked hypophosphatemia alters phosphate responsiveness of bone cells.Semantic proximity Read ↗

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