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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 nephropathy model. Further mechanistic analyses suggested that the inhibitory effects of FGF1 ΔHBS  on oxidative stress and inflammation were mediated by activation of the GSK-3β/Nrf2 pathway and inhibition of the ASK1/JNK signaling pathway, respectively. An in-depth study demonstrated that both pathways are under control of PI3K/AKT signaling activated by FGF1 ΔHBS . This finding expands the potential uses of FGF1 ΔHBS  for the treatment of various kinds of CKD associated with oxidative stress and inflammation.

FGF1ΔHBS ameliorates chronic kidney disease via PI3K/AKT mediated suppression of oxidative stress and inflammation