[Thioredoxin and atherosclerosis]

Increasing evidence has indicated that the modulation of intracellular redox states has marked influence on cellular events such as proliferation, activation, growth inhibition and death via the regulation of intracellular signal transduction and gene expression. Thioredoxin(TRX) is a multifunctional stress-inducible protein which protects cells from various types of stresses. TRX shows not only scavenging activity for ROS, but also regulating activity for various intracellular molecules including transcription factors. Overexpression of TRX in transgenic mice attenuates adriamycin-induced cardiotoxicity by reducing oxidative stresses. We demonstrated that serum TRX levels are correlated with the severity of heart failure, and are negatively correlated with left ventricular ejection fractions in patients with heart failure. Moreover, we found that the serum TRX levels in patients with ACS were significantly higher than in SA, whereas no significant difference was found between patients with SA and control subjects. The expression of TRX is enhanced not only in endothelial cells and macrophages in the human atherosclerotic plaques, but also in balloon-injured rat arteries. These findings suggest that TRX and the redox system modulated by TRX play an important role in the cellular defense against oxidative stress in cardiovascular diseases including the progression of atherosclerosis.