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本文引用的文献

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Inhibiting microRNA-192 ameliorates renal fibrosis in diabetic nephropathy.抑制 microRNA-192 可改善糖尿病肾病中的肾纤维化。
J Am Soc Nephrol. 2012 Mar;23(3):458-69. doi: 10.1681/ASN.2011050485. Epub 2012 Jan 5.
2
Circulating microRNAs as potential markers of human drug-induced liver injury.循环 microRNAs 作为人类药物性肝损伤潜在标志物的研究
Hepatology. 2011 Nov;54(5):1767-76. doi: 10.1002/hep.24538.
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Low-dose paclitaxel ameliorates fibrosis in the remnant kidney model by down-regulating miR-192.低剂量紫杉醇通过下调 miR-192 改善残肾模型中的纤维化。
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Cell adhesion-dependent control of microRNA decay.细胞黏附依赖性的 microRNA 降解调控。
Mol Cell. 2011 Sep 16;43(6):1005-14. doi: 10.1016/j.molcel.2011.07.031.
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Circulating microRNA expression is reduced in chronic kidney disease.循环 microRNA 表达在慢性肾脏病中降低。
Nephrol Dial Transplant. 2011 Nov;26(11):3794-802. doi: 10.1093/ndt/gfr485. Epub 2011 Sep 2.
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Smad3-mediated upregulation of miR-21 promotes renal fibrosis.Smad3 介导的 miR-21 上调促进肾纤维化。
J Am Soc Nephrol. 2011 Sep;22(9):1668-81. doi: 10.1681/ASN.2010111168. Epub 2011 Aug 18.
7
TGF-β/Smad3 signaling promotes renal fibrosis by inhibiting miR-29.TGF-β/Smad3 信号通路通过抑制 miR-29 促进肾纤维化。
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8
MicroRNA-21 orchestrates high glucose-induced signals to TOR complex 1, resulting in renal cell pathology in diabetes.微小 RNA-21 调控高糖诱导的信号转导至 TOR 复合物 1,导致糖尿病中的肾脏细胞病变。
J Biol Chem. 2011 Jul 22;286(29):25586-603. doi: 10.1074/jbc.M110.208066. Epub 2011 May 25.
9
p53 regulates epithelial-mesenchymal transition through microRNAs targeting ZEB1 and ZEB2.p53 通过靶向 ZEB1 和 ZEB2 的 microRNAs 调节上皮-间充质转化。
J Exp Med. 2011 May 9;208(5):875-83. doi: 10.1084/jem.20110235. Epub 2011 Apr 25.
10
A microRNA circuit mediates transforming growth factor-β1 autoregulation in renal glomerular mesangial cells.微小 RNA 电路介导转化生长因子-β1 在肾肾小球系膜细胞中的自身调控。
Kidney Int. 2011 Aug;80(4):358-68. doi: 10.1038/ki.2011.43. Epub 2011 Mar 9.

微小 RNA 电路在转化生长因子-β 作用和糖尿病肾病中的作用。

MicroRNA circuits in transforming growth factor-β actions and diabetic nephropathy.

机构信息

Department of Diabetes, Beckman Research Institute of City of Hope, Duarte, CA 91010, USA.

出版信息

Semin Nephrol. 2012 May;32(3):253-60. doi: 10.1016/j.semnephrol.2012.04.004.

DOI:10.1016/j.semnephrol.2012.04.004
PMID:22835456
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3407375/
Abstract

Diabetes is associated with significantly increased rates of kidney disease or diabetic nephropathy (DN), a severe microvascular complication that can lead to end-stage renal disease. End-stage renal disease needs to be treated by dialysis or kidney transplantation and also is associated with cardiovascular disease and macrovascular complications. Therefore, effective renal protection is critical to reduce the rates of mortality associated with diabetes. Although key signal transduction and gene regulation mechanisms have been identified and several drugs are currently in clinical use, the rates of DN are still escalating, suggesting the imperative need to identify new biomarkers and drug targets. The recent discovery of microRNAs (miRNAs) and their cellular functions provide an opportunity to fill these critical gaps. Because miRNAs can modulate the actions of key factors involved in DN such as transforming growth factor-β, they could be novel targets for the treatment of DN. This review covers the recent studies on the roles of miRNAs and miRNA circuits in transforming growth factor-β actions and in DN.

摘要

糖尿病与肾脏疾病或糖尿病肾病(DN)的发生率显著增加有关,DN 是一种严重的微血管并发症,可导致终末期肾病。终末期肾病需要通过透析或肾移植来治疗,而且还与心血管疾病和大血管并发症有关。因此,有效的肾脏保护对于降低与糖尿病相关的死亡率至关重要。尽管已经确定了关键的信号转导和基因调控机制,并且目前有几种药物在临床应用中,但 DN 的发病率仍在不断上升,这表明迫切需要确定新的生物标志物和药物靶点。最近发现的 microRNAs(miRNAs)及其细胞功能为填补这些关键空白提供了机会。由于 miRNAs 可以调节参与 DN 的关键因素的作用,例如转化生长因子-β,因此它们可能成为治疗 DN 的新靶点。这篇综述涵盖了 miRNAs 和 miRNA 回路在转化生长因子-β作用和 DN 中的最新研究。