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10.1007/s40618-014-0158-6

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suck abstract from ncbi


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pmid25194425
      J+Endocrinol+Invest 2014 ; 37 (11 ): 1121-6
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  • Alpha Klotho and phosphate homeostasis #MMPMID25194425
  • Bian A ; Xing C ; Hu MC
  • J Endocrinol Invest 2014[Nov]; 37 (11 ): 1121-6 PMID25194425 show ga
  • The Klotho family consists of three single-pass transmembrane proteins??Klotho, ?Klotho and ?Klotho. Each of them combines with fibroblast growth factor (FGF) receptors (FGFRs) to form receptor complexes for various FGF?s. ?Klotho is a co-receptor for physiological FGF23 signaling and appears essential for FGF23-mediated regulation of mineral metabolism. ?Klotho protein also plays a FGF23-independent role in phosphate homeostasis. Animal experimental studies and clinical observations have demonstrated that ?Klotho deficiency leads to severe hyperphosphatemia; moderate elevation of ?Klotho reduces serum phosphate and extremely high ?Klotho induces hypophosphatemia and high-FGF23. ?Klotho maintains circulating phosphate in a narrow range by modulating intestinal phosphate absorption, urinary phosphate excretion by the kidney, and phosphate distribution into bone rather than soft tissue in concerted interaction with other calciophosphotropic hormones such as PTH, FGF23, and 1,25-(OH)(2) vitamin D. The role of ?Klotho in maintenance of phosphate homeostasis is mediated by direct suppression of Na-dependent phosphate cotransporters in target organs. Therefore, ?Klotho manipulation may be a novel strategy for genetic and acquired phosphate disorders and for medical conditions with ?Klotho deficiency such as chronic kidney disease in future.
  • |Animals [MESH]
  • |Biological Transport/physiology [MESH]
  • |Cardiovascular Diseases/diagnosis/metabolism [MESH]
  • |Glucuronidase/*metabolism [MESH]
  • |Homeostasis/*physiology [MESH]
  • |Humans [MESH]
  • |Klotho Proteins [MESH]


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