Fibroblast Growth Factor 23–Mediated Bone Disease - 15/12/17
Doi : 10.1016/j.ecl.2016.09.013
Anda R. Gonciulea, MD, Suzanne M. Jan De Beur, MD ⁎ 
Division of Endocrinology, Diabetes and Metabolism, Johns Hopkins University School of Medicine, Baltimore, MD, USA
∗Corresponding author. 5200 Eastern Avenue, Mason F. Lord Center Tower, Suite 4300, Baltimore, MD 21224.5200 Eastern AvenueMason F. Lord Center TowerSuite 4300BaltimoreMD21224
Résumé |
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.
Le texte complet de cet article est disponible en PDF.Keywords : FGF23, α-Klotho, Hypophosphatemia, Hyperphosphatemia, Rickets, Osteomalacia
Plan
| Disclosures: Dr A.R. Gonciulea has no conflict of interests. Dr S.M. Jan de Beur is site PI for clinical trials for KRN23 in tumor-induced osteomalacia and X-linked hypophosphatemic rickets and is a consultant to Ultragenyx. |
© 2016
Elsevier Inc. Tous droits réservés.
Vol 46 - N° 1
P. 19-39 - mars 2017 Retour au numéro
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