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

ABSTRACT:

Background

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.

Results

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 fib

SUBMITTER: Zhang X 

PROVIDER: S-EPMC5975516 | biostudies-literature | 2018 May

REPOSITORIES: biostudies-literature