SHIP, a novel factor to ameliorate extracellular matrix accumulation via suppressing PI3K/Akt/CTGF signaling in diabetic kidney disease

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• 作者：Fan Li ; Lisha Li ; Meijuan Cheng ; Xiumin Wang ; Jun Hao ; Shuxia Liu ; Huijun Duan ; ^{duanhuijun@hotmail.com}
• 关键词：SHIP ; Diabetic kidney disease ; PI3K/Akt ; Extracellular matrix ; Renal tubular cell
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2017
• 出版时间：22 January 2017
• 年：2017
• 卷：482
• 期：4
• 页码：1477-1483
• 全文大小：2895 K
• 卷排序：482

文摘

SHIP decreases in kidneys of diabetic mice concomitant with increased phospho-Akt, CTGF and extracellular matrix deposit. High glucose decreases SHIP expression and increases phospho-Akt, CTGF and collagen I in HK2 cells. Upregulation of SHIP prevented extracellular matrix deposit of diabetic kidney disease.