Abstract
Excessive reactive oxygen species (ROS) play a key role in the pathogenesis of diabetic cardiac disease. While increased ROS are traditionally viewed as arising from the metabolic flux of diabetes, we explored the possibility that altered expression of anti-oxidant systems may also contribute, focusing on tissue activity of the thioredoxin reducing system, and tissue expression of its endogenous inhibitor thioredoxin interating protein (TxnIP).
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