Fibroblast growth factor 23: fueling the fire
Mark Hanudel1, Harald Jüppner2, Isidro B Salusky1
1Division of Pediatric Nephrology, David Geffen School of Medicine at University of California-Los Angeles, Los Angeles, California, USA.
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.
Related Concept Videos
Introduction to Fibroblasts
TGF - β Signaling Pathway
Regulation of Angiogenesis and Blood Supply
Role of Hematopoietic Growth Factors
Thrombopoietin (TPO), mainly released by the liver,...


