NDT Advance Access originally published online on July 19, 2005
Nephrology Dialysis Transplantation 2005 20(10):2032-2035; doi:10.1093/ndt/gfh991
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org
Editorial Comment
FGF-23, vitamin D and calcification: the unholy triad
1 Department of Oral and Developmental Biology, Harvard School of Dental Medicine, Boston, MA, USA,2 Genetics Unit, Shriners Hospital for Children, Montreal, Quebec, Canada and 3 Department of Pathology, Nagasaki University School of Biomedical Sciences, Nagasaki, Japan
Correspondence and offprint requests to: Mohammed S. Razzaque, Department of Oral and Developmental Biology, Research and Educational Building, Room 312, Harvard School of Dental of Medicine, 190 Longwood Ave, Boston, MA 02115, USA. Email: mrazzaque@hms.harvard.edu
Keywords: fibroblast growth factor 23 (FGF-23); hyperphosphatemia; soft tissue calcification; vitamin D
| The first 150 words of the full text of this article appear below. |
 |
Introduction |
|---|
Recent studies have changed the commonly held view that phosphate is mostly needed for normal skeletal growth and development. Extensive research in the last decade has identified numerous other essential dynamic functions for phosphate, ranging from signalling to energy metabolism. Abnormal phosphate homeostasis potentially affects functional activities of almost any organ system. Despite its wide biological importance and significance, the regulation of phosphate homeostasis is not yet clearly understood. Recent studies have identified a number of molecules with phosphaturic activities, including fibroblast growth factor-23 (FGF-23) [1], frizzled-related protein 4 [2] and matrix extracellular phosphoglycoprotein [1,3]. Among these recently identified molecules, so far FGF-23 has been implicated in various human diseases, including autosomal dominant hypophosphatemic rickets (ADHR) [4], oncogenic osteomalacia (OOM) [5], X-linked hypophosphatemia (XLH) [6], chronic renal diseases [7] and familial tumoral calcinosis (FTC)
|
Phosphate homeostasis |
|---|
|
FGF-23 |
|---|
|
Soft tissue calcification |
|---|
|
FGF-23 and soft tissue calcification |
|---|
Fgf-23 null animals
Fgf-23/1
(OH)ase null animals |
Conclusion |
|---|
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  T. Nakatani, M. Ohnishi, and M. S. Razzaque Inactivation of klotho function induces hyperphosphatemia even in presence of high serum fibroblast growth factor 23 levels in a genetically engineered hypophosphatemic (Hyp) mouse model FASEB J, November 1, 2009; 23(11): 3702 - 3711. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Mizobuchi, D. Towler, and E. Slatopolsky Vascular Calcification: The Killer of Patients with Chronic Kidney Disease J. Am. Soc. Nephrol., July 1, 2009; 20(7): 1453 - 1464. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. S. Razzaque FGF23-mediated regulation of systemic phosphate homeostasis: is Klotho an essential player? Am J Physiol Renal Physiol, March 1, 2009; 296(3): F470 - F476. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Nakatani, B. Sarraj, M. Ohnishi, M. J. Densmore, T. Taguchi, R. Goetz, M. Mohammadi, B. Lanske, and M. S. Razzaque In vivo genetic evidence for klotho-dependent, fibroblast growth factor 23 (Fgf23) -mediated regulation of systemic phosphate homeostasis FASEB J, February 1, 2009; 23(2): 433 - 441. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. S. Razzaque Does FGF23 toxicity influence the outcome of chronic kidney disease? Nephrol. Dial. Transplant., January 1, 2009; 24(1): 4 - 7. [Full Text] [PDF]
|
|
|
|
 |
|
 D. Medici, M. S. Razzaque, S. DeLuca, T. L. Rector, B. Hou, K. Kang, R. Goetz, M. Mohammadi, M. Kuro-o, B. R. Olsen, et al. FGF-23-Klotho signaling stimulates proliferation and prevents vitamin D-induced apoptosis J. Cell Biol., August 11, 2008; 182(3): 459 - 465. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. A. Towler Vascular Calcification: A Perspective On An Imminent Disease Epidemic IBMS BoneKEy, February 1, 2008; 5(2): 41 - 58. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. S Razzaque and B. Lanske The emerging role of the fibroblast growth factor-23-klotho axis in renal regulation of phosphate homeostasis J. Endocrinol., July 1, 2007; 194(1): 1 - 10. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Stompor AN OVERVIEW OF THE PATHOPHYSIOLOGY OF VASCULAR CALCIFICATION IN CHRONIC KIDNEY DISEASE Perit. Dial. Int., June 1, 2007; 27(Supplement_2): S215 - S222. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Sitara, M. S. Razzaque, R. St-Arnaud, W. Huang, T. Taguchi, R. G. Erben, and B. Lanske Genetic Ablation of Vitamin D Activation Pathway Reverses Biochemical and Skeletal Anomalies in Fgf-23-Null Animals Am. J. Pathol., December 1, 2006; 169(6): 2161 - 2170. [Abstract] [Full Text] [PDF]
|
|