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Papers published by Dr Nianxiu Tian:
Original Research
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Astragaloside IV represses high glucose-induced mesangial cells activation by enhancing autophagy via SIRT1 deacetylation of NF-κB P65 subunit
![](cr_data/cache/submission_images/s174000/174058/12_sep_2018_174058_fig6_200_200_90.jpg)
Wang X, Gao Y, Tian N, Zhu Z, Wang T, Xu J, Wu B, Zhang N
Drug Design, Development and Therapy 2018, 12:2971-2980
Published Date: 12 September 2018
Original Research
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Astragaloside IV improves renal function and fibrosis via inhibition of miR-21-induced podocyte dedifferentiation and mesangial cell activation in diabetic mice
![](cr_data/cache/submission_images/s170000/170840/06_aug_2018_170840_fig10_200_200_90.jpg)
Wang X, Gao Y, Tian N, Zou D, Shi Y, Zhang N
Drug Design, Development and Therapy 2018, 12:2431-2442
Published Date: 6 August 2018
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.](assets/img/article_icons/noteworthy.png)
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Emodin mitigates podocytes apoptosis induced by endoplasmic reticulum stress through the inhibition of the PERK pathway in diabetic nephropathy
Tian N, Gao Y, Wang X, Wu X, Zou D, Zhu Z, Han ZJ, Wang T, Shi Y
Drug Design, Development and Therapy 2018, 12:2195-2211
Published Date: 13 July 2018