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FGF23 and disorders of phosphate homeostasis.
Cytokine Growth Factor Rev. 2005 Apr; 16(2):221-32.CG

Abstract

It is well known that fibroblast growth factor (FGF) family members are associated with embryonic development and are critical for basic metabolic functions. This review will focus upon fibroblast growth factor-23 (FGF23) and its roles in disorders associated with phosphate handling. The discovery that mutations in FGF23 were responsible for the isolated renal phosphate wasting disorder autosomal dominant hypophosphatemic rickets (ADHR) has ascribed novel functions to the FGF family. FGF23 circulates in the bloodstream, and animal models demonstrate that FGF23 controls phosphate and Vitamin D homeostasis through the regulation of specific renal proteins. The ADHR mutations in FGF23 produce a protein species less susceptible to proteolytic processing. X-linked hypophosphatemic rickets (XLH), tumor-induced osteomalacia (TIO), and fibrous dysplasia of bone (FD) are disorders involving phosphate homeostasis that share phenotypes with ADHR, indicating that FGF23 may be a common denominator for the pathophysiology of these syndromes. Our understanding of FGF23 will help to develop novel therapies for phosphate wasting disorders, as well as for disorders of increased serum phosphate, such as tumoral calcinosis, a rare disorder, and renal failure, a common disorder.

Authors+Show Affiliations

Department of Medical and Molecular Genetics, Indiana University School of Medicine, 975 West Walnut St., IB130, Indianapolis, IN 46202, USA.No affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Review

Language

eng

PubMed ID

15863037

Citation

Yu, Xijie, and Kenneth E. White. "FGF23 and Disorders of Phosphate Homeostasis." Cytokine & Growth Factor Reviews, vol. 16, no. 2, 2005, pp. 221-32.
Yu X, White KE. FGF23 and disorders of phosphate homeostasis. Cytokine Growth Factor Rev. 2005;16(2):221-32.
Yu, X., & White, K. E. (2005). FGF23 and disorders of phosphate homeostasis. Cytokine & Growth Factor Reviews, 16(2), 221-32.
Yu X, White KE. FGF23 and Disorders of Phosphate Homeostasis. Cytokine Growth Factor Rev. 2005;16(2):221-32. PubMed PMID: 15863037.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - FGF23 and disorders of phosphate homeostasis. AU - Yu,Xijie, AU - White,Kenneth E, Y1 - 2005/02/05/ PY - 2005/5/3/pubmed PY - 2005/8/17/medline PY - 2005/5/3/entrez SP - 221 EP - 32 JF - Cytokine & growth factor reviews JO - Cytokine Growth Factor Rev VL - 16 IS - 2 N2 - It is well known that fibroblast growth factor (FGF) family members are associated with embryonic development and are critical for basic metabolic functions. This review will focus upon fibroblast growth factor-23 (FGF23) and its roles in disorders associated with phosphate handling. The discovery that mutations in FGF23 were responsible for the isolated renal phosphate wasting disorder autosomal dominant hypophosphatemic rickets (ADHR) has ascribed novel functions to the FGF family. FGF23 circulates in the bloodstream, and animal models demonstrate that FGF23 controls phosphate and Vitamin D homeostasis through the regulation of specific renal proteins. The ADHR mutations in FGF23 produce a protein species less susceptible to proteolytic processing. X-linked hypophosphatemic rickets (XLH), tumor-induced osteomalacia (TIO), and fibrous dysplasia of bone (FD) are disorders involving phosphate homeostasis that share phenotypes with ADHR, indicating that FGF23 may be a common denominator for the pathophysiology of these syndromes. Our understanding of FGF23 will help to develop novel therapies for phosphate wasting disorders, as well as for disorders of increased serum phosphate, such as tumoral calcinosis, a rare disorder, and renal failure, a common disorder. SN - 1359-6101 UR - https://www.unboundmedicine.com/medline/citation/15863037/FGF23_and_disorders_of_phosphate_homeostasis_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1359-6101(05)00003-1 DB - PRIME DP - Unbound Medicine ER -