Effects of klotho deletion from bone during chronic kidney disease.

Abstract

Klotho is a type I transmembrane protein that acts as a permissive co-receptor for FGF23 and helps to maintain proper mineral metabolism. Mice carrying a loss-of-function mutation in either the Klotho or Fgf23 gene develop many similar phenotypes including osteoporosis. Based on these observations it was hypothesized that the bone phenotypes in Klotho- and Fgf23-null mice may be mediated through a common signaling pathway. Recent improvements in antibody specificity have shown that osteoblasts and osteocytes, which produce FGF23, also express low amount of membrane Klotho. But, the role of Klotho in bone is still largely unclear. In this review we summarize the literature and show that Klotho has an FGF23 dependent and independent effect in bone.