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Novel functions of circulating Klotho.

Julia M Hum1, Linda O'Bryan2, Rosamund C Smith2

  • 1Department of Medical and Molecular Genetics, Division of Molecular Genetics and Gene Therapy, Indiana University School of Medicine, Indianapolis, IN 46202, USA; Division of Biomedical Science, Marian University School of Osteopathic Medicine, Indianapolis, IN 46222, USA.

Bone
|November 29, 2016
PubMed
Summary

Studies on rare mineral metabolism diseases reveal αKlotho (αKL) and FGF23 functions. Extended delivery of cleaved αKlotho (cKL) in mouse models shows promise for treating chronic kidney disease-mineral bone disorder (CKD-MBD).

Keywords:
FGF23HyperphosphatemiaHypophosphatemiaPhosphateVascular calcificationcKL

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Area of Science:

  • Mineral metabolism
  • Endocrinology
  • Nephrology

Background:

  • Rare diseases of mineral metabolism have elucidated key biological functions of αKlotho (αKL) and Fibroblast growth factor-23 (FGF23).
  • These insights have significant implications for prevalent conditions like chronic kidney disease-mineral bone disorder (CKD-MBD).
  • αKL primarily regulates mineral homeostasis in the kidney as a co-receptor for FGF23.

Purpose of the Study:

  • To review recent findings on the role of cleaved αKlotho (cKL) as a circulating factor.
  • To examine the effects of extended cKL delivery in mouse models mimicking CKD-MBD phenotypes.

Main Methods:

  • Review of studies involving extended delivery of cleaved αKlotho (cKL).
  • Utilized mouse models exhibiting phenotypes relevant to CKD-MBD.

Main Results:

  • Emerging data highlight αKL's function beyond its co-receptor role, acting as a cleaved circulating factor (cKL).
  • Extended cKL delivery in mouse models demonstrated therapeutic potential for CKD-MBD related phenotypes.

Conclusions:

  • Cleaved αKlotho (cKL) represents a potential therapeutic avenue for CKD-MBD.
  • Further research into cKL's biological functions and therapeutic applications is warranted.