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• W2034649336 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." @default.
• W2034649336 created "2016-06-24" @default.
• W2034649336 creator A5031267390 @default.
• W2034649336 creator A5056261958 @default.
• W2034649336 date "2005-04-01" @default.
• W2034649336 modified "2023-10-16" @default.
• W2034649336 title "FGF23 and disorders of phosphate homeostasis" @default.
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• W2034649336 doi "https://doi.org/10.1016/j.cytogfr.2005.01.002" @default.
• W2034649336 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15863037" @default.
• W2034649336 hasPublicationYear "2005" @default.
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