HOME HELP CONTACT US SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (12) Citing Articles via Google Scholar Google Scholar Articles by Razzaque, M. S Articles by Lanske, B. Search for Related Content PubMed PubMed Citation Articles by Razzaque, M. S Articles by Lanske, B.

Department of Developmental Biology, Harvard School of Dental Medicine, Research and Education Building, Room # 304, 190 Longwood Avenue, Boston, Massachusetts 02115, USA

(Requests for offprints should be addressed to M S Razzaque; Email: mrazzaque{at}hms.harvard.edu)

Normal mineral ion homeostasis is tightly controlled by numerous endocrine factors that coordinately exert effects on intestine, kidney, and bone to maintain physiological balance. The importance of the fibroblast growth factor (FGF)-23–klotho axis in regulating mineral ion homeostasis has been proposed from recent research observations. Experimental studies suggest that 1) FGF23 is an important in vivo regulator of phosphate homeostasis, 2) FGF23 acts as a counter regulatory hormone to modulate the renal 1-hydroxylase and sodium–phosphate cotransporter activities, 3) there is a trend of interrelationship between FGF23 and parathyroid hormone activities, 4) most of the FGF23 functions are conducted through the activation of FGF receptors, and 5) such receptor activation needs klotho, as a cofactor to generate downstream signaling events. These observations clearly suggest the emerging roles of the FGF23–klotho axis in maintaining mineral ion homeostasis. In this brief article, we will summarize how the FGF23–klotho axis might coordinately regulate normal mineral ion homeostasis, and how their abnormal regulation could severely disrupt such homeostasis to induce disease pathology.

This article has been cited by other articles:

				C. A. Brownstein, J. Zhang, A. Stillman, B. Ellis, N. Troiano, D. J. Adams, C. M. Gundberg, R. P. Lifton, and T. O. Carpenter Increased Bone Volume and Correction of HYP Mouse Hypophosphatemia in the Klotho/HYP Mouse Endocrinology, February 1, 2010; 151(2): 492 - 501. [Abstract] [Full Text] [PDF]

				U. M. Polanska, L. Duchesne, J. C. Harries, D. G. Fernig, and T. K. Kinnunen N-Glycosylation Regulates Fibroblast Growth Factor Receptor/EGL-15 Activity in Caenorhabditis elegans in Vivo J. Biol. Chem., November 27, 2009; 284(48): 33030 - 33039. [Abstract] [Full Text] [PDF]

				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]

				H. Eddington and J. G. Heaf Clinical management of disturbances of calcium and phosphate metabolism in dialysis patients NDT Plus, August 1, 2009; 2(4): 267 - 272. [Abstract] [Full Text] [PDF]

				B. J. Schouten, P. J. Hunt, J. H. Livesey, C. M. Frampton, and S. G. Soule FGF23 Elevation and Hypophosphatemia after Intravenous Iron Polymaltose: A Prospective Study J. Clin. Endocrinol. Metab., July 1, 2009; 94(7): 2332 - 2337. [Abstract] [Full Text] [PDF]

				S.-K. Cha, M.-C. Hu, H. Kurosu, M. Kuro-o, O. Moe, and C.-L. Huang Regulation of Renal Outer Medullary Potassium Channel and Renal K+ Excretion by Klotho Mol. Pharmacol., July 1, 2009; 76(1): 38 - 46. [Abstract] [Full Text] [PDF]

				L. Masi, A. Gozzini, A. Franchi, D. Campanacci, A. Amedei, A. Falchetti, F. Franceschelli, G. Marcucci, A. Tanini, R. Capanna, et al. A Novel Recessive Mutation of Fibroblast Growth Factor-23 in Tumoral Calcinosis J. Bone Joint Surg. Am., May 1, 2009; 91(5): 1190 - 1198. [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]

				J. Danziger The bone-renal axis in early chronic kidney disease: an emerging paradigm Nephrol. Dial. Transplant., September 1, 2008; 23(9): 2733 - 2737. [Full Text] [PDF]

				L. L. Demer and Y. Tintut Vascular Calcification: Pathobiology of a Multifaceted Disease Circulation, June 3, 2008; 117(22): 2938 - 2948. [Full Text] [PDF]

				M. S. Razzaque Can patient-specific stem cell therapy enhance renal repair? Nephrol. Dial. Transplant., June 1, 2008; 23(6): 1826 - 1830. [Full Text] [PDF]

				M. S. Razzaque Klotho and Na+,K+-ATPase activity: solving the calcium metabolism dilemma? Nephrol. Dial. Transplant., February 1, 2008; 23(2): 459 - 461. [Full Text] [PDF]