title: Fibroblast growth factor 23: fueling the fire.
abstract: In chronic kidney disease, systemic inflammation is common and associated with mortality. The present study demonstrates that fibroblast growth factor 23 (FGF23) contributes to uremic inflammation by increasing hepatic expression and secretion of inflammatory cytokines. FGF23 binds to hepatic FGFR4, inducing calcineurin/nuclear factor of activated T-cell signaling, resulting in increased expression of interleukin 6 and C-reactive protein. The proinflammatory effects of FGF23 are inhibited by an isoform-specific FGFR4 blocking antibody and by cyclosporine, a calcineurin inhibitor.
authors.affiliation: Division of Pediatric Nephrology, David Geffen School of Medicine at University of California-Los Angeles, Los Angeles, California, USA.
authors.forename: Mark
authors.initials: M
authors.lastname: Hanudel
authors.affiliation: Endocrine Unit and Division of Pediatric Nephrology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.
authors.forename: Harald
authors.initials: H
authors.lastname: Jüppner
authors.affiliation: Division of Pediatric Nephrology, David Geffen School of Medicine at University of California-Los Angeles, Los Angeles, California, USA. Electronic address: isalusky@mednet.ucla.edu.
authors.forename: Isidro B
authors.initials: IB
authors.lastname: Salusky
mesh_terms: D000089703:Fibroblast Growth Factor-23; D005346:Fibroblast Growth Factors; D022781:Hepatocytes; D006801:Humans; D007249:Inflammation; D051436:Renal Insufficiency, Chronic
chemical_list: C000717427:FGF23 protein, human; D005346:Fibroblast Growth Factors; D000089703:Fibroblast Growth Factor-23