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Ren Fail. 2017 Nov;39(1):306-313. doi: 10.1080/0886022X.2016.1274662.
2
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本文引用的文献

1
Atg5-mediated autophagy deficiency in proximal tubules promotes cell cycle G2/M arrest and renal fibrosis.Atg5 介导的近端肾小管自噬缺陷促进细胞周期 G2/M 期阻滞和肾纤维化。
Autophagy. 2016 Sep;12(9):1472-86. doi: 10.1080/15548627.2016.1190071. Epub 2016 Jun 15.
2
Persistent activation of autophagy in kidney tubular cells promotes renal interstitial fibrosis during unilateral ureteral obstruction.单侧输尿管梗阻期间,肾小管细胞中自噬的持续激活会促进肾间质纤维化。
Autophagy. 2016 Jun 2;12(6):976-98. doi: 10.1080/15548627.2016.1166317. Epub 2016 Apr 28.
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Reactive oxygen species-initiated autophagy opposes aldosterone-induced podocyte injury.活性氧引发的自噬对抗醛固酮诱导的足细胞损伤。
Am J Physiol Renal Physiol. 2016 Apr 1;310(7):F669-F678. doi: 10.1152/ajprenal.00409.2015. Epub 2016 Jan 13.
4
The roles of oxidative stress, endoplasmic reticulum stress, and autophagy in aldosterone/mineralocorticoid receptor-induced podocyte injury.氧化应激、内质网应激和自噬在醛固酮/盐皮质激素受体诱导的足细胞损伤中的作用。
Lab Invest. 2015 Dec;95(12):1374-86. doi: 10.1038/labinvest.2015.118. Epub 2015 Sep 28.
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Inactivated Sendai virus induces apoptosis and autophagy via the PI3K/Akt/mTOR/p70S6K pathway in human non-small cell lung cancer cells.灭活仙台病毒通过PI3K/Akt/mTOR/p70S6K信号通路诱导人非小细胞肺癌细胞凋亡和自噬。
Biochem Biophys Res Commun. 2015 Sep 11;465(1):64-70. doi: 10.1016/j.bbrc.2015.07.130. Epub 2015 Jul 30.
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Methodology used in studies reporting chronic kidney disease prevalence: a systematic literature review.报告慢性肾脏病患病率的研究中所使用的方法:一项系统文献综述
Nephrol Dial Transplant. 2015 Aug;30 Suppl 4(Suppl 4):iv6-16. doi: 10.1093/ndt/gfv131.
7
(Pro)renin receptor regulates autophagy and apoptosis in podocytes exposed to high glucose.(前)肾素受体调节暴露于高糖环境下的足细胞中的自噬和凋亡。
Am J Physiol Endocrinol Metab. 2015 Aug 1;309(3):E302-10. doi: 10.1152/ajpendo.00603.2014. Epub 2015 Jun 16.
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Oxidative stress in chronic kidney disease.慢性肾脏病中的氧化应激
Iran J Kidney Dis. 2015 May;9(3):165-79.
9
Ursolic acid attenuates diabetic mesangial cell injury through the up-regulation of autophagy via miRNA-21/PTEN/Akt/mTOR suppression.熊果酸通过抑制miRNA-21/PTEN/Akt/mTOR上调自噬,减轻糖尿病肾小球系膜细胞损伤。
PLoS One. 2015 Feb 17;10(2):e0117400. doi: 10.1371/journal.pone.0117400. eCollection 2015.
10
Oxidative stress and autophagy: crucial modulators of kidney injury.氧化应激与自噬:肾损伤的关键调节因子
Redox Biol. 2015;4:208-14. doi: 10.1016/j.redox.2015.01.001. Epub 2015 Jan 13.

自噬在慢性肾脏病中的研究进展

Advance of autophagy in chronic kidney diseases.

作者信息

Deng Xu, Xie Yifan, Zhang Aihua

机构信息

a Department of Nephrology , Children's Hospital of Nanjing Medical University , Nanjing , China.

b Jiangsu Key Laboratory of Pediatrics , Nanjing Medical University , Nanjing , China.

出版信息

Ren Fail. 2017 Nov;39(1):306-313. doi: 10.1080/0886022X.2016.1274662.

DOI:10.1080/0886022X.2016.1274662
PMID:28085532
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6014530/
Abstract

Autophagy, a highly conserved mechanism for cell survival, emerges as an important pathway in many biological processes and diseases conditions. Studies of cultured renal cells, human kidney tissues and experimental animal models implicate that autophagy regulation is the critical aspects in chronic kidney diseases (CKD). Here, we summarize the current studies on the role of autophagy in CKD. Unveiling the precise regulation mechanism of autophagy in CKD is essential for developing potential prevention, diagnostic and therapeutic targets of these sticky clinical challenges.

摘要

自噬是一种高度保守的细胞存活机制,在许多生物学过程和疾病状态中成为一条重要途径。对培养的肾细胞、人类肾脏组织和实验动物模型的研究表明,自噬调节是慢性肾脏病(CKD)的关键方面。在此,我们总结了目前关于自噬在CKD中作用的研究。揭示CKD中自噬的精确调节机制对于开发应对这些棘手临床挑战的潜在预防、诊断和治疗靶点至关重要。