| First Author | Ren Y | Year | 2010 |
| Journal | FEBS Lett | Volume | 584 |
| Issue | 15 | Pages | 3480-5 |
| PubMed ID | 20624390 | Mgi Jnum | J:163475 |
| Mgi Id | MGI:4822087 | Doi | 10.1016/j.febslet.2010.07.010 |
| Citation | Ren Y, et al. (2010) p38 MAPK pathway is involved in high glucose-induced thioredoxin interacting protein induction in mouse mesangial cells. FEBS Lett 584(15):3480-5 |
| abstractText | 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. |
