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浏览/检索结果: 共4条，第1-4条 帮助 限定条件 专题：中南大学    第一署名单位    第一作者单位    通讯作者单位     已选(0)清除 条数/页：5101520253035404550556065707580859095100   排序方式：请选择作者升序作者降序题名升序题名降序发表日期升序发表日期降序提交时间升序提交时间降序 Persistent activation of autophagy in kidney tubular cells promotes renal interstitial fibrosis during unilateral ureteral obstruction 期刊论文 Autophagy, 2016, 卷号: 12, 期号: 6, 页码: 976-998 作者:  Livingston, Man J;  Ding, Han-Fei;  Huang, Shuang;  Hill, Joseph A;  Yin, Xiao-Ming 收藏  |  浏览/下载：5/0  |  提交时间：2019/12/03 Autophagy  kidney injury  proximal tubule  renal fibrosis  unilateral ureteral obstruction   Mefunidone Attenuates Tubulointerstitial Fibrosis in a Rat Model of Unilateral Ureteral Obstruction 期刊论文 PLOS ONE, 2015, 卷号: 10, 期号: 6, 页码: e0129283 作者:  Liu, Chunyan;  Mei, Wenjuan;  Tang, Juan;  Yuan, Qiongjing;  Huang, Ling 收藏  |  浏览/下载：12/0  |  提交时间：2019/12/03 Kidneys,Collagens,Fibrosis,Macrophages,Inflammation,Transcription factors,Fibroblasts,Phosphorylation   Increased adenosine levels contribute to ischemic kidney fibrosis in the unilateral ureteral obstruction model 期刊论文 Experimental and Therapeutic Medicine, 2015, 卷号: 9, 期号: 3, 页码: 737-743 作者:  Tang, Jin;  Jiang, Xianzhen;  Zhou, Yihong;  Xia, Bing;  Dai, Yingbo* 收藏  |  浏览/下载：3/0  |  提交时间：2019/12/03 adenosine  cytokines  renal interstitial fibrosis  unilateral ureteral obstruction model  alpha-smooth muscle actin   Paclitaxel attenuates renal interstitial fibroblast activation and interstitial fibrosis by inhibiting STAT3 signaling 期刊论文 Drug Design, Development and Therapy, 2015, 卷号: 9, 页码: 2139-2148 作者:  Zhang, Lei;  Xu, Xuan;  Yang, Ruhao;  Chen, Jingwen;  Wang, Shixuan 收藏  |  浏览/下载：4/0  |  提交时间：2019/12/03 Recent studies have demonstrated that paclitaxel might inhibit renal fibrosis. However  the underlying molecular mechanism remains unclear. In this study  we hypothesized that low-dose paclitaxel may block the STAT3 (signal transducer and activator of transcription 3) signaling to attenuate fibrosis in a mouse model with unilateral ureteral obstruction. Both NRK-49F cells and mice with unilateral ureteral obstruction were treated with paclitaxel. The results showed that paclitaxel treatment resulted in a dose- and time-dependent decrease in tyrosine-phosphorylated STAT3  and inhibited the expression of fibronectin  alpha-smooth muscle actin (α-SMA)  and collagen I in cultured NRK-49F cells. S3I-201  an STAT3 inhibitor  also suppressed the expression of fibronectin  α-SMA  and collagen I in cultured NRK-49F cells. Mechanistically  paclitaxel treatment blocked the STAT3 activity by disrupting the association of STAT3 with tubulin and inhibiting STAT3 nucleus translocation. Furthermore  paclitaxel also ameliorated renal fibrosis by down-regulating the expression of fibronectin  α-SMA  and collagen I  and suppressed the infiltration of macrophages and production of TNF-α  IL-1β  TGF-β  and ICAM-1 (intercellular adhesion molecule 1) by inhibition of STAT3 activity in obstructive nephropathy. These results suggest that paclitaxel may block the STAT3 activity by disrupting the association of STAT3 with tubulin and inhibiting STAT3 nucleus translocation  consequently leading to the suppression of renal interstitial fibroblast activation and the development of renal fibrosis  and inhibition of proinflammatory cytokine production.