Exogenous thioredoxin reduces inflammation in autoimmune myocarditis.

Levels of reactive oxygen species (ROS) are tightly regulated in mammalian cells. A variety of enzymes produce ROS, including NAD(P)H oxidase, xanthine oxidase, glucose oxidase, myeloperoxidase, the family of nitric oxide synthases, and mitochondrial enzymes.1–4 Low levels of ROS such as superoxide or hydrogen peroxide regulate highly specific targets.5,6 In the cardiovascular system, for example, ROS serve as signaling molecules, mediating vascular endothelial growth factor signal transduction, activating matrix metalloproteinases, and regulating cell cycle phosphatases. Host defenses that protect against oxidative stress include small antioxidant molecules such as ascorbate, -tocopherol, glutathione, and thioredoxin (Trx), as well as antioxidant enzymes such as superoxide dismutase, catalase, paraoxonase, glutathione reductase, glutathione peroxidase, and Trx reductase.