The FGF23 and Klotho system beyond mineral metabolism

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• 作者：Makoto Kuro-o
• 关键词：FGF23 ; αKlotho ; Phosphatopathy
• 刊名：Clinical and Experimental Nephrology
• 出版年：2017
• 出版时间：March 2017
• 年：2017
• 卷：21
• 期：1-supp
• 页码：64-69
• 全文大小：
• 刊物类别：Medicine
• 刊物主题：Nephrology; Urology;
• 出版者：Springer Japan
• ISSN：1437-7799
• 卷排序：21

文摘

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.