NDT Advance Access originally published online on November 7, 2008
Nephrology Dialysis Transplantation 2009 24(1):4-7; doi:10.1093/ndt/gfn620
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© The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org
Does FGF23 toxicity influence the outcome of chronic kidney disease?
Department of Developmental Biology, Harvard School of Dental Medicine, Boston, MA, USA
M. Shawkat Razzaque, Department of Developmental Biology, Harvard School of Dental Medicine, Research and Education Building, Room # 304, 190 Longwood Avenue, Boston, MA 02115, USA. Tel: +1-617-432-5768; Fax: +617-432-5767; E-mail: mrazzaque@hms.harvard.edu; razzaquems@yahoo.com
Keywords: CKD; FGF23; phosphate homeostasis; vitamin D
| The first 150 words of the full text of this article appear below. |
| Fibroblast growth factor-23 (FGF23) |
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Maintenance of physiologic phosphate balance is important for essential cellular functions [1]. Dysregulation of the phosphate balance in the form of hypophosphataemia can lead to the development of myopathy, cardiac dysfunction, haematological abnormalities and bone mineralization defects [1]. In contrast, hyperphosphataemia can cause vascular and soft tissue calcification [2,3]. Studies have convincingly demonstrated that FGF23 is a master regulator of systemic phosphate homeostasis [4–9].
FGF23 is a 30 kDa protein that is proteolytically processed to generate smaller N-terminal (
18 kDa) and C-terminal (
12 kDa) fragments. The N-terminal fragment of FGF23 contains the FGF receptor-binding domain, while the C-terminal fragment is proposed to be necessary for interaction with Klotho (a type 1 membrane protein with homology to ß-glucosidase), which is believed to be a cofactor in FGF23–FGF receptor interactions [10]. FGF23 is a circulating phosphaturic factor that controls systemic
| FGF23 and CKD |
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| Elevated serum FGF23 and mortality |
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| Concluding remarks |
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This article has been cited by other articles:
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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] |
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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] |
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