| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 10954084 | Journal of Molecular and Cellular Cardiology | 2011 | 9 Pages |
Abstract
⺠Trx1 attenuates oxidative stress, apoptosis, fibrosis and increases neovascularization during myocardial infarction (MI). ⺠Trx1 reduces the expression of TXNIP and AKAP12 during MI. ⺠Trx1 increases the expression of p-Akt, p-GSK-3beta, Beta-catenin, HIF-1alpha, VEGF, p-eNOS, Bcl-2 and survivin during MI. ⺠Trx1 reduces/prevents the post-infarction mediated ventricular remodeling.
Keywords
LVIDsAKAP12hypoxia inducible factor alphaTXNIPTBARSLVIDdTMIHIF-1αWMITrx1Myocardial infarctionVentricular remodelingOxidative stressThioredoxin-1Thioredoxin 1Apoptosisstandard error meanVascular endothelial growth factorVascular Endothelial Growth Factor (VEGF)LADSEMthiobarbituric acid reactive substancesNeovascularizationThioredoxin interacting proteinleft anterior descending coronary artery
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Authors
Ram Sudheer Adluri, Mahesh Thirunavukkarasu, Lijun Zhan, Yuzo Akita, Samson Mathews Samuel, Hajime Otani, Ye-Shih Ho, Gautam Maulik, Nilanjana Maulik,