Fibroblast Growth Factor 23-Mediated Bone Disease

Anda R Gonciulea; Suzanne M Jan De Beur

doi:10.1016/j.ecl.2016.09.013

Fibroblast Growth Factor 23-Mediated Bone Disease

Endocrinol Metab Clin North Am. 2017 Mar;46(1):19-39. doi: 10.1016/j.ecl.2016.09.013. Epub 2016 Dec 14.

Authors

Anda R Gonciulea¹, Suzanne M Jan De Beur²

Affiliations

¹ Division of Endocrinology, Diabetes and Metabolism, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
² Division of Endocrinology, Diabetes and Metabolism, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Electronic address: sjandebe@jhmi.edu.

PMID: 28131132
DOI: 10.1016/j.ecl.2016.09.013

Abstract

Fibroblast growth factor 23 (FGF23) is an important regulator of phosphate and vitamin D metabolism and its excessive or insufficient production leads to a wide variety of skeletal disorders. This article reviews the FGF23-α-Klotho signaling pathway, highlighting the latest developments in FGF23 regulation and action, and describes the disorders associated with FGF23 excess or deficiency.

Keywords: FGF23; Hyperphosphatemia; Hypophosphatemia; Osteomalacia; Rickets; α-Klotho.

Publication types

Review

MeSH terms

Bone Diseases / metabolism*
Fibroblast Growth Factor-23
Fibroblast Growth Factors / metabolism*
Glucuronidase / metabolism*
Humans
Klotho Proteins
Phosphates / metabolism
Signal Transduction*
Vitamin D / metabolism

Substances

FGF23 protein, human
Phosphates
Vitamin D
Fibroblast Growth Factors
Fibroblast Growth Factor-23
Glucuronidase
Klotho Proteins