FGF23^C-tail improves diabetic nephropathy by attenuating renal fibrosis and inflammation

High level of serum fibroblast growth factor 23 (FGF23) is implicated in the development and progression of diabetic nephropathy (DN), making it a crucial factor in the pathogenesis of DN. FGF23 is also tightly correlated with inflammation in the progression of DN. The aim of this study was to explore whether the C-terminal of FGF23 (FGF23^C-tail), an antagonist that can block the FGF23 signaling pathway by competing with intact FGF23, could exhibit a therapeutic effect on DN.

Biochemical data and histological examination showed that FGF23 ^C-tail administration ameliorated the functional and morphological abnormalities of db/db mice with DN without changing the levels of circulating FGF23 and phosphate. Evaluation of morphology and fibrosis by Masson's trichrome staining and IHC staining of fibronectin, PCR, and western blot analysis showed that FGF23^C-tail prevents diabetes-induced fibrosis in db/db mice. Importantly, FGF23^C-tail decreased the levels of inflammatory cytokines in serum and renal tissues.

FGF23^C-tail may improve diabetic nephropathy by decreasing inflammation and fibrosis in db/db mice, suggesting that blocking of FGF23 action remains an important therapeutic target for the prevention or attenuation of the progression of DN.