Display Settings:

Format

Send to:

Choose Destination
We are sorry, but NCBI web applications do not support your browser and may not function properly. More information
Curr Opin Nephrol Hypertens. 2006 Jul;15(4):437-41.

Klotho as a regulator of fibroblast growth factor signaling and phosphate/calcium metabolism.

Author information

  • Department of Pathology, The University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75390-9072, USA. makoto.kuro-o@utsouthwestern.edu

Abstract

PURPOSE OF REVIEW:

This review summarizes the most recent findings on Klotho in the regulation of fibroblast growth factor-23 (FGF23) signaling and phosphate/calcium homeostasis.

RECENT FINDINGS:

The klotho gene encodes a single-pass transmembrane protein and functions as an aging-suppressor gene, which extends life span when overexpressed and accelerates the development of aging-like phenotypes when disrupted in mice. FGF23 is a hormone that suppresses phosphate reabsorption in renal proximal tubules. Recent studies have shown that Klotho mice and Fgf23 mice exhibit identical phenotypes including hyperphosphatemia and hypercalcemia in addition to the aging-like syndrome. This may be explained by the fact that Klotho binds to multiple FGF receptors and increases their affinity to FGF23. Another Klotho protein function is to activate transient receptor potential vanilloid-5 - a calcium channel involved in calcium reabsorption in the kidney. Klotho protein can modify sugar chains on transient receptor potential vanilloid-5 through its activity as a beta-glucuronidase, preventing the calcium channel from internalization and inactivation.

SUMMARY:

Klotho protein binds to fibroblast growth factor receptors and functions as a regulator of FGF23 signaling. It also functions as an enzyme that modifies sugar chains of transient receptor potential vanilloid-5 and regulates its activity. Klotho is a multi-functional protein that regulates phosphate/calcium metabolism as well as aging.

PMID:
16775459
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Lippincott Williams & Wilkins
    Loading ...
    Write to the Help Desk