p38 MAPK pathway is involved in high glucose-induced thioredoxin interacting protein induction in mouse mesangial cells

FEBS Letters
Yunzhuo RenHuijun Duan

Abstract

Excessive reactive oxygen species (ROS) play a key role in the pathogenesis of diabetic nephropathy. The thioredoxin (TRX) system, a major thiol antioxidant system, regulates the reduction of intracellular ROS. Here we show that high glucose (HG) inhibits TRX ROS-scavenging function through p38 mitogen-activated protein kinase (MAPK)-mediated induction of thioredoxin interacting protein (TXNIP) in mouse mesangial cells (MMCs). Knockdown of TXNIP in MMCs reversed HG-induced reduction of TRX activity and inhibited HG-induced activation of p38 MAPK and increased synthesis of TGF-beta1 and fibronectin. These data suggest that HG-induced overexpression of TXNIP in MMCs, which may be via the p38 MAPK pathway.

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Citations

May 23, 2012·Antioxidants & Redox Signaling·Samuel LeeRichard T Lee
Jan 17, 2012·Journal of Clinical Biochemistry and Nutrition·Hiroshi MasutaniJunji Yodoi
Sep 13, 2015·Molecular and Cellular Endocrinology·Haijiang WuHuijun Duan
Jul 5, 2016·International Journal of Molecular Sciences·Shudong WangYang Zheng
Jun 30, 2011·American Journal of Physiology. Endocrinology and Metabolism·Howard GoldbergI George Fantus
Jan 13, 2018·International Journal of Molecular Medicine·Jinying WeiHuijun Duan
Dec 12, 2020·International Journal of Molecular Sciences·Haruka TsubakiDouglas Gordon Walker
Aug 25, 2018·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Wenwei XuYaoming Xue

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