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Original Research

Noteworthy comment: The study indicated that emodin treatment ameliorates urine albumin, serum creatinine and blood urea nitrogen as well as pathological kidney damages of diabetic nephropathy KK-Ay mice. Such therapeutic effects of emodin may be resulted from emodin-induced reduction of ER stress and podocytes apoptosis by inhibiting the PERK-eIF2α signaling pathway. Emodin reduced expression of podocytes apoptosis and ER-stress marker GRP78, ATF4, CHOP, and phosphorylated PERK and eIF2a in vivo. Ex vivo experiments also showed that emodin decreases GRP78 which is induced by high glucose or tunicamycin. RNAi assays with shRNAs against emodin and PERK confirmed the results in vivo. The study suggested the potential application of emodin in diabetic nephropathy therapy.

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Emodin mitigates podocytes apoptosis induced by endoplasmic reticulum stress through the inhibition of the PERK pathway in diabetic nephropathy

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