Secreted Klotho and chronic kidney disease

Ming C Hu, Makoto Kuro-o, Orson W Moe

Research output: Chapter in Book/Report/Conference proceedingChapter

77 Scopus citations

Abstract

Soluble Klotho (sKl) in the circulation can be generated directly by alterative splicing of the Klotho transcript or the extracellular domain of membrane Klotho can be released from membrane-anchored Klotho on the cell surface. Unlike membrane Klotho which functions as a coreceptor for fibroblast growth factor-23 (FGF23), sKl, acts as hormonal factor and plays important roles in anti-aging, anti-oxidation, modulation of ion transport, and Wnt signaling. Emerging evidence reveals that Klotho deficiency is an early biomarker for chronic kidney diseases as well as a pathogenic factor. Klotho deficiency is associated with progression and chronic complications in chronic kidney disease including vascular calcification, cardiac hypertrophy, and secondary hyperparathyroidism. In multiple experimental models, replacement of sKl, or manipulated up-regulation of endogenous Klotho protect the kidney from renal insults, preserve kidney function, and suppress renal fibrosis, in chronic kidney disease. Klotho is a highly promising candidate on the horizon as an early biomarker, and as a novel therapeutic agent for chronic kidney disease.

Original languageEnglish (US)
Title of host publicationEndocrine FGFs and Klothos
Pages126-157
Number of pages32
DOIs
StatePublished - 2012

Publication series

NameAdvances in Experimental Medicine and Biology
Volume728
ISSN (Print)0065-2598

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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    Hu, M. C., Kuro-o, M., & Moe, O. W. (2012). Secreted Klotho and chronic kidney disease. In Endocrine FGFs and Klothos (pp. 126-157). (Advances in Experimental Medicine and Biology; Vol. 728). https://doi.org/10.1007/978-1-4614-0887-1_9