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.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Ren Y,Shi Y,Wang Y,Li Y,Wu S,Li H,Zhang Y,Duan Hdoi
10.1016/j.febslet.2010.07.010subject
Has Abstractpub_date
2010-08-04 00:00:00pages
3480-5issue
15eissn
0014-5793issn
1873-3468pii
S0014-5793(10)00565-Xjournal_volume
584pub_type
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