title: Enhanced induction of Cyp24a1 by FGF23 but low serum 24,25-dihydroxyvitamin D in CKD: implications for therapy.
abstract: In normal people, induction by FGF23 of renal Cyp24a1, the enzyme that degrades 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D, helps to protect from the disorders caused by excessive 1,25-dihydroxyvitamin D. Dai and co-workers report, however, that in human and mouse kidney disease, high FGF23 concurs with low rather than high serum 24,25-dihydroxyvitamin D, a biomarker of Cyp24a1 activity. Their characterization of the underlying mechanisms provides new understanding of how kidney disease impairs the health benefits of vitamin D-FGF23/klotho interactions.
authors.affiliation: Experimental Nephrology Laboratory, IRBLleida (Lleida Institute for Biomedical Research), Lleida School of Medicine, Universidad de Lleida, Lleida, Spain. adusso@irblleida.cat
authors.forename: Adriana S
authors.initials: AS
authors.lastname: Dusso
authors.forename: Mariano
authors.initials: M
authors.lastname: Rodriguez
mesh_terms: D000818:Animals; D004100:Dihydroxycholecalciferols / Q000097:blood*; D005260:Female; D000089703:Fibroblast Growth Factor-23; D005346:Fibroblast Growth Factors / Q000097:blood*; D006801:Humans; D008297:Male; D009394:Nephritis, Hereditary / Q000097:blood*; D051436:Renal Insufficiency, Chronic / Q000097:blood*
chemical_list: D004100:Dihydroxycholecalciferols; C000717427:FGF23 protein, human; C000717428:Fgf23 protein, mouse; D005346:Fibroblast Growth Factors; D000089703:Fibroblast Growth Factor-23