Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10815356 | Cellular Signalling | 2013 | 13 Pages |
Abstract
⺠High glucose induces endothelial dysfunction via Nox4/ROS/CIKS/NF-κB/AP-1. ⺠Targeting CIKS blunts HG induced adhesion molecule and cytokine expression. ⺠AGEs, oxLDL and AOPPs induce CIKS-dependent endothelial dysfunction. ⺠Type 1 diabetic animals express high levels of CIKS in the aorta in vivo. ⺠CIKS is a novel therapeutic target in diabetic vascular complications.
Keywords
LOX-1DCFH-DANEMOIκBAP-1dichlorofluoresceinDPIRAGEIRFTRAFoxLDLIKKTRAF3IP2CIKSAct1SAPKc-jun amino-terminal kinase2′,7′-dichlorofluorescin-diacetatecopGFPTNFUTRHSANF-κBNADPHDcfshRNAGSTJnkMMPAOPPsC/EBPIκB kinaseMOINOxSmall interfering RNAsmall hairpin RNAROSsiRNAhuman serum albuminEndothelial dysfunctionNADPH oxidaseinterleukinOxidative stressdiphenylene iodoniumAgeIFN regulatory factorTNF receptor associated factordominant negativetumor necrosis factornuclear factor kappa Boxidized low density lipoproteinmatrix metalloproteinaseadvanced oxidation protein productsNF-κB essential modulatoruntranslated regioninhibitory κBwild-typenicotinamide adenine dinucleotide phosphateHyperglycemiaCCAAT/enhancer-binding proteinactivator protein-1Stress-activated protein kinaseadvanced glycation end productmultiplicity of infectionglutathione-S-transferaseReactive oxygen speciesreceptor for AGELectin-like oxidized low-density lipoprotein receptor-1
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Authors
Balachandar Venkatesan, Anthony J. Valente, Nitin A. Das, Andrea J. Carpenter, Tadashi Yoshida, Jean-Luc Delafontaine, Ulrich Siebenlist, Bysani Chandrasekar,