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Reciprocal control of 1,25-dihydroxyvitamin D and FGF23 formation involving the FGF23/Klotho system.
Clin J Am Soc Nephrol. 2010 Sep; 5(9):1717-22.CJ

Abstract

Fibroblast growth factor 23 (FGF23) is a circulating hormone that is synthesized by osteocytes and osteoblasts. This glycosylated peptide controls phosphate balance by modulating urinary phosphate excretion and indirectly intestinal phosphate absorption by reducing expression of the renal and intestinal sodium phosphate transporters. In a feedback loop, 1,25-dihydroxyvitamin D and phosphate intake control FGF23 production. FGF23 is inactivated by cleavage by a still unidentified enzyme. FGF23 cleavage occurs within cells and probably in the circulation. Klotho, a protein expressed at the cell surface of few organs, forms complexes with FGF receptors, which increases their affinity for FGF23. Klotho is also released into the plasma and urine by an enzymatic cleavage. FGF23 plays a central role in vitamin D metabolism: It inhibits calcitriol synthesis in the kidney and stimulates the catabolism of active vitamin D sterols. In turn, calcitriol stimulates FGF23 and Klotho expression. In chronic kidney diseases, FGF23 concentration increases as GFR declines, whereas Klotho tissue expression decreases. The modifications of FGF23 and Klotho expression are probably involved in the genesis of hyperparathyroidism and the resistance to vitamin D receptor (VDR) activation in chronic kidney disease. Low vitamin D, high FGF23 concentrations, and defects in VDR activation are associated with similar risks, which evoke the possibility that potential FGF23 toxicity might be partly mediated by FGF23-induced decrease in calcitriol or 25-hydroxyvitamin D. Conversely, VDR activators could be used to modulate Klotho or FGF23 expression.

Authors+Show Affiliations

Service des Explorations Fonctionnelles, Université Paris Descartes, Faculté de Médecine, INSERM U845, Hôpital Necker-Enfants Malades, Paris, France. dominique.prie@inserm.frNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

20798257

Citation

Prié, Dominique, and Gérard Friedlander. "Reciprocal Control of 1,25-dihydroxyvitamin D and FGF23 Formation Involving the FGF23/Klotho System." Clinical Journal of the American Society of Nephrology : CJASN, vol. 5, no. 9, 2010, pp. 1717-22.
Prié D, Friedlander G. Reciprocal control of 1,25-dihydroxyvitamin D and FGF23 formation involving the FGF23/Klotho system. Clin J Am Soc Nephrol. 2010;5(9):1717-22.
Prié, D., & Friedlander, G. (2010). Reciprocal control of 1,25-dihydroxyvitamin D and FGF23 formation involving the FGF23/Klotho system. Clinical Journal of the American Society of Nephrology : CJASN, 5(9), 1717-22. https://doi.org/10.2215/CJN.02680310
Prié D, Friedlander G. Reciprocal Control of 1,25-dihydroxyvitamin D and FGF23 Formation Involving the FGF23/Klotho System. Clin J Am Soc Nephrol. 2010;5(9):1717-22. PubMed PMID: 20798257.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Reciprocal control of 1,25-dihydroxyvitamin D and FGF23 formation involving the FGF23/Klotho system. AU - Prié,Dominique, AU - Friedlander,Gérard, Y1 - 2010/08/26/ PY - 2010/8/28/entrez PY - 2010/8/28/pubmed PY - 2011/1/12/medline SP - 1717 EP - 22 JF - Clinical journal of the American Society of Nephrology : CJASN JO - Clin J Am Soc Nephrol VL - 5 IS - 9 N2 - Fibroblast growth factor 23 (FGF23) is a circulating hormone that is synthesized by osteocytes and osteoblasts. This glycosylated peptide controls phosphate balance by modulating urinary phosphate excretion and indirectly intestinal phosphate absorption by reducing expression of the renal and intestinal sodium phosphate transporters. In a feedback loop, 1,25-dihydroxyvitamin D and phosphate intake control FGF23 production. FGF23 is inactivated by cleavage by a still unidentified enzyme. FGF23 cleavage occurs within cells and probably in the circulation. Klotho, a protein expressed at the cell surface of few organs, forms complexes with FGF receptors, which increases their affinity for FGF23. Klotho is also released into the plasma and urine by an enzymatic cleavage. FGF23 plays a central role in vitamin D metabolism: It inhibits calcitriol synthesis in the kidney and stimulates the catabolism of active vitamin D sterols. In turn, calcitriol stimulates FGF23 and Klotho expression. In chronic kidney diseases, FGF23 concentration increases as GFR declines, whereas Klotho tissue expression decreases. The modifications of FGF23 and Klotho expression are probably involved in the genesis of hyperparathyroidism and the resistance to vitamin D receptor (VDR) activation in chronic kidney disease. Low vitamin D, high FGF23 concentrations, and defects in VDR activation are associated with similar risks, which evoke the possibility that potential FGF23 toxicity might be partly mediated by FGF23-induced decrease in calcitriol or 25-hydroxyvitamin D. Conversely, VDR activators could be used to modulate Klotho or FGF23 expression. SN - 1555-905X UR - https://www.unboundmedicine.com/medline/citation/20798257/Reciprocal_control_of_125_dihydroxyvitamin_D_and_FGF23_formation_involving_the_FGF23/Klotho_system_ L2 - https://cjasn.asnjournals.org/cgi/pmidlookup?view=long&pmid=20798257 DB - PRIME DP - Unbound Medicine ER -