Over-nutrition contributes to tubulointerstitial fibrosis by targeting nutrient-sensing kinases: role for the mTOR/S6K pathway.
作者信息
Nistala Ravi, Sowers James R, Whaley-Connell Adam
出版信息
Cell Cycle. 2012 Mar 1;11(5):831-2. doi: 10.4161/cc.11.5.19588.
Abstract
摘要
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Over-nutrition contributes to tubulointerstitial fibrosis by targeting nutrient-sensing kinases: role for the mTOR/S6K pathway.营养过剩通过作用于营养感应激酶导致肾小管间质纤维化：mTOR/S6K信号通路的作用
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本文引用的文献
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The Impact of Overnutrition on Insulin Metabolic Signaling in the Heart and the Kidney.营养过剩对心脏和肾脏胰岛素代谢信号的影响。
Cardiorenal Med. 2011;1(2):102-112. doi: 10.1159/000327140. Epub 2011 Apr 15.
2
Cellular and molecular mechanisms of renal fibrosis.肾脏纤维化的细胞和分子机制。
Nat Rev Nephrol. 2011 Oct 18;7(12):684-96. doi: 10.1038/nrneph.2011.149.
3
Angiotensin II activation of mTOR results in tubulointerstitial fibrosis through loss of N-cadherin.血管紧张素 II 激活 mTOR 导致 N-钙黏蛋白丢失，从而引起肾小管间质纤维化。
Am J Nephrol. 2011;34(2):115-25. doi: 10.1159/000329327. Epub 2011 Jun 29.
4
High-carbohydrate, high-fat diet-induced metabolic syndrome and cardiovascular remodeling in rats.高碳水化合物高脂肪饮食诱导的大鼠代谢综合征和心血管重构。
J Cardiovasc Pharmacol. 2011 May;57(5):611-24. doi: 10.1097/FJC.0b013e31821b1379.
5
Albumin-induced epithelial-mesenchymal transition and ER stress are regulated through a common ROS-c-Src kinase-mTOR pathway: effect of imatinib mesylate.白蛋白诱导的上皮-间充质转化和内质网应激通过一个共同的 ROS-c-Src 激酶-mTOR 途径调节：甲磺酸伊马替尼的作用。
Am J Physiol Renal Physiol. 2011 May;300(5):F1214-22. doi: 10.1152/ajprenal.00710.2010. Epub 2011 Mar 2.
6
Dietary fructose causes tubulointerstitial injury in the normal rat kidney.膳食果糖可导致正常大鼠肾脏的肾小管间质性损伤。
Am J Physiol Renal Physiol. 2010 Mar;298(3):F712-20. doi: 10.1152/ajprenal.00433.2009. Epub 2010 Jan 13.
7
Fructose, but not dextrose, accelerates the progression of chronic kidney disease.果糖而非葡萄糖会加速慢性肾病的进展。
Am J Physiol Renal Physiol. 2007 Oct;293(4):F1256-61. doi: 10.1152/ajprenal.00181.2007. Epub 2007 Aug 1.
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Nature. 2004 Sep 9;431(7005):200-5. doi: 10.1038/nature02866. Epub 2004 Aug 11.
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Exp Cell Res. 2004 Jun 10;296(2):183-95. doi: 10.1016/j.yexcr.2003.12.032.
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Disruption of cadherin/catenin expression, localization, and interactions during HgCl2-induced nephrotoxicity.氯化汞诱导肾毒性过程中钙黏蛋白/连环蛋白表达、定位及相互作用的破坏。
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