FEBS Lett 2010,
PMID: 20624390
Ren, Yunzhuo; Shi, Yonghong; Wang, Yuehua; Li, Yingmin; Wu, Shuhui; Li, Hang; Zhang, Yanling; Duan, Huijun
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.
Diseases/Pathways annotated by Medline MESH: MAP Kinase Signaling System
Document information provided by NCBI PubMed
Text Mining Data
TGF-beta1 → TRX: "
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
"
TRX → MAPK: "
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
"
Manually curated Databases
No curated data.