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Published in: Clinical and Experimental Nephrology 1/2017

01-03-2017 | Review article

The FGF23 and Klotho system beyond mineral metabolism

Author: Makoto Kuro-o

Published in: Clinical and Experimental Nephrology | Special Issue 1/2017

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Abstract

FGF23 is a bone-derived hormone that acts primarily on the kidney to induce phosphaturia and suppress synthesis of 1,25-dihydroxyvitamin D3. The unique feature of FGF23 is that it requires Klotho as an obligate co-receptor. The FGF23–Klotho system has emerged as an endocrine axis indispensable for maintaining phosphate homeostasis. Mineral and bone disorders associated with chronic kidney disease (CKD-MBD) can be viewed as a series of events triggered by a compensatory response of the FGF23–Klotho system to excess phosphate intake relative to the residual nephron number. Furthermore, the fact that disruption of the FGF23–Klotho system causes phosphate retention and a syndrome resembling aging in mammals has led to the notion that phosphate accelerates aging. The aging-like pathology caused by phosphate, or phosphatopathy, may be unique to the higher organisms having the Klotho gene and provides new insights into the molecular mechanism of aging in humans.
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Metadata
Title
The FGF23 and Klotho system beyond mineral metabolism
Author
Makoto Kuro-o
Publication date
01-03-2017
Publisher
Springer Japan
Published in
Clinical and Experimental Nephrology / Issue Special Issue 1/2017
Print ISSN: 1342-1751
Electronic ISSN: 1437-7799
DOI
https://doi.org/10.1007/s10157-016-1357-6

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