Several Nrf2 activators are at various stages of clinical development and are being tested in clinical trials for chronic kidney disease (CKD) including diabetic kidney disease, Alport syndrome, autosomal dominant polycystic kidney disease and focal segmental glomerulosclerosis.
Sitagliptin may induce HO-1 expression via activation of PI3K and Nrf2 in rats with diabetic nephropathy; HO-1 can improve the oxidative stress of diabetic nephropathy, eventually protect from diabetic nephropathy.
Taken together, our results indicate that PHLPP1 up-surged Nrf2 nuclear instability by promoting Nrf2/β-TrCP association and its inhibition may be critical in the management of diabetic nephropathy.
The aim of this study was to evaluate the renoprotective effects of hesperetin against DN in rats, and to investigate mechanisms from the aspect of Nrf2/ARE/Glo-1 pathway.
Therefore, it is suggested that SZGB can restrain epithelial-mesenchymal transition (EMT) through stimulating the Nrf2 pathway, which improves renal interstitial fibrosis in DN.
These findings demonstrated that BA exhibited a protective effect on diabetic nephropathy in STZ-induced rats possibly through the AMPK/NF-κB/Nrf2 pathway.
These results suggest for the first time that FF prevents the development of DN via up-regulating FGF21 and stimulating PI3K/Akt/GSK-3β/Fyn-mediated activation of the Nrf2 pathway.
This study was aimed at exploring whether AST exerts a protective effect on DN via activating nuclear factor erythroid 2-related factor 2- (Nrf2-) antioxidative response element (ARE) signaling.
Thus, these results suggest that CGA is a potential therapeutic agent in the treatment of DN due to its antioxidant and anti-inflammatory effects which are mediated via the modulation of the Nrf2/HO-1 and NF-ĸB pathways.
Whereas, whether PD could resist DN through regulating CKIP-1 and consequently promoting the activation of Nrf2-ARE pathway needs further investigation.