Fibroblast growth factor 23 and bone mineralisation

doi:10.1038/ijos.2015.1

Review

. 2015 Mar 23;7(1):8-13.

doi: 10.1038/ijos.2015.1.

Fibroblast growth factor 23 and bone mineralisation

Yu-Chen Guo¹, Quan Yuan¹

Affiliations

PMID: 25655009
PMCID: PMC4817534
DOI: 10.1038/ijos.2015.1

Review

Fibroblast growth factor 23 and bone mineralisation

Yu-Chen Guo et al. Int J Oral Sci. 2015.

. 2015 Mar 23;7(1):8-13.

doi: 10.1038/ijos.2015.1.

Authors

Yu-Chen Guo¹, Quan Yuan¹

Affiliation

¹ State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.

PMID: 25655009
PMCID: PMC4817534
DOI: 10.1038/ijos.2015.1

Abstract

Fibroblast growth factor 23 (FGF23) is a hormone that is mainly secreted by osteocytes and osteoblasts in bone. The critical role of FGF23 in mineral ion homeostasis was first identified in human genetic and acquired rachitic diseases and has been further characterised in animal models. Recent studies have revealed that the levels of FGF23 increase significantly at the very early stages of chronic kidney disease (CKD) and may play a critical role in mineral ion disorders and bone metabolism in these patients. Our recent publications have also shown that FGF23 and its cofactor, Klotho, may play an independent role in directly regulating bone mineralisation instead of producing a systematic effect. In this review, we will discuss the new role of FGF23 in bone mineralisation and the pathophysiology of CKD-related bone disorders.

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References

1. Shimada T, Kakitani M, Yamazaki Y et al. Targeted ablation of Fgf23 demonstrates an essential physiological role of FGF23 in phosphate and vitamin D metabolism. J Clin Invest 2004; 113(4): 561–568. - PMC - PubMed
1. Sitara D, Razzaque MS, Hesse M et al. Homozygous ablation of fibroblast growth factor-23 results in hyperphosphatemia and impaired skeletogenesis, and reverses hypophosphatemia in Phex-deficient mice. Matrix Biol 2004; 23(7): 421–432. - PMC - PubMed
1. Bergwitz C, Jüppner H. Regulation of phosphate homeostasis by PTH, vitamin D, and FGF23. Annu Rev Med 2010; 61: 91–104. - PMC - PubMed
1. ADHR Consortium. Autosomal dominant hypophosphataemic rickets is associated with mutations in FGF23. Nat Genet 2000; 26(3): 345–348. - PubMed
1. Shimada T, Mizutani S, Muto T et al. Cloning and characterization of FGF23 as a causative factor of tumor-induced osteomalacia. Proc Natl Acad Sci U S A 2001; 98(11): 6500–6505. - PMC - PubMed

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[1] Shimada T, Kakitani M, Yamazaki Y et al. Targeted ablation of Fgf23 demonstrates an essential physiological role of FGF23 in phosphate and vitamin D metabolism. J Clin Invest 2004; 113(4): 561–568. - PMC - PubMed

[2] Shimada T, Kakitani M, Yamazaki Y et al. Targeted ablation of Fgf23 demonstrates an essential physiological role of FGF23 in phosphate and vitamin D metabolism. J Clin Invest 2004; 113(4): 561–568. - PMC - PubMed

[3] Sitara D, Razzaque MS, Hesse M et al. Homozygous ablation of fibroblast growth factor-23 results in hyperphosphatemia and impaired skeletogenesis, and reverses hypophosphatemia in Phex-deficient mice. Matrix Biol 2004; 23(7): 421–432. - PMC - PubMed

[4] Sitara D, Razzaque MS, Hesse M et al. Homozygous ablation of fibroblast growth factor-23 results in hyperphosphatemia and impaired skeletogenesis, and reverses hypophosphatemia in Phex-deficient mice. Matrix Biol 2004; 23(7): 421–432. - PMC - PubMed

[5] Bergwitz C, Jüppner H. Regulation of phosphate homeostasis by PTH, vitamin D, and FGF23. Annu Rev Med 2010; 61: 91–104. - PMC - PubMed

[6] Bergwitz C, Jüppner H. Regulation of phosphate homeostasis by PTH, vitamin D, and FGF23. Annu Rev Med 2010; 61: 91–104. - PMC - PubMed

[7] ADHR Consortium. Autosomal dominant hypophosphataemic rickets is associated with mutations in FGF23. Nat Genet 2000; 26(3): 345–348. - PubMed

[8] ADHR Consortium. Autosomal dominant hypophosphataemic rickets is associated with mutations in FGF23. Nat Genet 2000; 26(3): 345–348. - PubMed

[9] Shimada T, Mizutani S, Muto T et al. Cloning and characterization of FGF23 as a causative factor of tumor-induced osteomalacia. Proc Natl Acad Sci U S A 2001; 98(11): 6500–6505. - PMC - PubMed

[10] Shimada T, Mizutani S, Muto T et al. Cloning and characterization of FGF23 as a causative factor of tumor-induced osteomalacia. Proc Natl Acad Sci U S A 2001; 98(11): 6500–6505. - PMC - PubMed

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Fibroblast growth factor 23 and bone mineralisation

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Fibroblast growth factor 23 and bone mineralisation

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