Pruning the ricket thicket.

Published

Journal Article

Overexpression of FGF23 results in hypophosphatemic rickets, which is characterized by renal phosphate wasting, inappropriately low circulating levels of the active form of vitamin D, and skeletal abnormalities. The precise mechanisms of how excess FGF23 leads to hypophosphatemic rickets are not clear. In this issue of the JCI, Bai and colleagues demonstrate that deletion or inhibition of CYP24A1, which initiates degradation of the active form of vitamin D, ameliorates skeletal abnormalities in two mouse models of hypophosphatemic rickets. While this work supports an important role for excess CYP24A1 activity in the pathogenesis of FGF23-mediated hypophosphatemic rickets, more work will need to be done before CYP24A1 inhibition can be integrated into the management of patients living with these diseases.

Full Text

Duke Authors

Cited Authors

  • David, V; Wolf, M

Published Date

  • February 2016

Published In

Volume / Issue

  • 126 / 2

Start / End Page

  • 473 - 476

PubMed ID

  • 26784540

Pubmed Central ID

  • 26784540

Electronic International Standard Serial Number (EISSN)

  • 1558-8238

Digital Object Identifier (DOI)

  • 10.1172/JCI85005

Language

  • eng

Conference Location

  • United States