FGF1^ΔHBS ameliorates chronic kidney disease via PI3K/AKT mediated suppression of oxidative stress and inflammation.

ABSTRACT: Currently, there is a lack of effective therapeutic approaches to the treatment of chronic kidney disease (CKD) with irreversible deterioration of renal function. This study aimed to investigate the ability of mutant FGF1 (FGF1^ΔHBS, which has reduced mitogenic activity) to alleviate CKD and to study its associated mechanisms. We found that FGF1^ΔHBS exhibited much weaker mitogenic activity than wild-type FGF1 (FGF1^WT) in renal tissues. RNA-seq analysis revealed that FGF1^ΔHBS inhibited oxidative stress and inflammatory signals in mouse podocytes challenged with high glucose. These antioxidative stress and anti-inflammatory activities of FGF1^ΔHBS prevented CKD in two mouse models: a diabetic nephropathy model and an adriamycin-induced nep

SUBMITTER: Wang D 

PROVIDER: S-EPMC6561918 | biostudies-literature | 2019 Jun

REPOSITORIES: biostudies-literature