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The FGF23/Klotho axis in the regulation of mineral and metabolic homeostasis.
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- Author(s): Kawai M
- Source:
Hormone molecular biology and clinical investigation [Horm Mol Biol Clin Investig] 2016 Oct 01; Vol. 28 (1), pp. 55-67.
- Publication Type:
Journal Article; Review
- Language:
English
- Additional Information
- Source:
Publisher: De Gruyter Country of Publication: Germany NLM ID: 101538885 Publication Model: Print Cited Medium: Internet ISSN: 1868-1891 (Electronic) Linking ISSN: 18681883 NLM ISO Abbreviation: Horm Mol Biol Clin Investig Subsets: MEDLINE
- Publication Information:
Original Publication: Berlin : De Gruyter
- Subject Terms:
- Abstract:
The function of fibroblast growth factor (FGF) 23 has been suggested to be multifaceted beyond its canonical function as a regulator of mineral metabolism. FGF23 was originally shown to play a central role in phosphate (Pi) and vitamin D metabolism, and a number of diseases associated with dysregulated Pi metabolism have been attributed to abnormal FGF23 signaling activities. The discovery of Klotho as a co-receptor for FGF23 signaling has also accelerated understanding on the molecular mechanisms underlying Pi and vitamin D metabolism. In addition to these canonical functions, FGF23 has recently been implicated in a number of metabolic diseases including chronic kidney disease-associated complications, cardiovascular diseases, and obesity-related disorders; however, the physiological significance and molecular mechanisms of these emerging roles of FGF23 remain largely unknown. Molecular and functional insights into the FGF23 pathway will be discussed in the present review, with an emphasis on its role in human disorders related to dysregulated Pi metabolism as well as metabolic disorders.
- Accession Number:
0 (FGF23 protein, human)
0 (Minerals)
62031-54-3 (Fibroblast Growth Factors)
7Q7P4S7RRE (Fibroblast Growth Factor-23)
EC 3.2.1.31 (Glucuronidase)
EC 3.2.1.31 (Klotho Proteins)
- Publication Date:
Date Created: 20160305 Date Completed: 20170314 Latest Revision: 20211204
- Publication Date:
20231215
- Accession Number:
10.1515/hmbci-2015-0068
- Accession Number:
26943611
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