Fibroblast growth factor 23: fueling the fire

Mark Hanudel; Harald Jüppner; Isidro B Salusky

doi:10.1016/j.kint.2016.08.013

Fibroblast growth factor 23: fueling the fire

Kidney Int. 2016 Nov;90(5):928-930. doi: 10.1016/j.kint.2016.08.013.

Authors

Mark Hanudel¹, Harald Jüppner², Isidro B Salusky³

Affiliations

¹ Division of Pediatric Nephrology, David Geffen School of Medicine at University of California-Los Angeles, Los Angeles, California, USA.
² Endocrine Unit and Division of Pediatric Nephrology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.
³ Division of Pediatric Nephrology, David Geffen School of Medicine at University of California-Los Angeles, Los Angeles, California, USA. Electronic address: [email protected].

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.

Publication types

Comment

MeSH terms

Fibroblast Growth Factor-23
Fibroblast Growth Factors*
Hepatocytes
Humans
Inflammation
Renal Insufficiency, Chronic*

Substances

FGF23 protein, human
Fibroblast Growth Factors
Fibroblast Growth Factor-23

Abstract

Publication types

MeSH terms

Substances

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