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Mitochondrial protection and the reversal of left ventricular remodeling.

eactive oxygen species (ROS) originate from many sources, including the Nox family of NADPH oxidases, xanthine oxidase, and mitochondria, in which superoxide radicals are the byproducts of oxidative energy production. Superoxide radicals are dismutated by superoxide dismutase (SOD), to produce hydrogen peroxides, which in turn are degraded into water and molecular oxygen by glutathione peroxidase and peroxiredoxin. Hydroxyl radicals (OH•), which are the most potent ROS, are formed from hydrogen peroxides through the Fenton reaction. There are no endogenous enzymes to eliminate these radicals. In healthy mitochondria, mitochondrial ROS are adequately scavenged by antioxidant enzymes, but in damaged mitochondria, energy production is decreased and ROS production is disproportionally increased, surpassing the endogenous antioxidant capacity. Mitochondrial oxidative stress is implicated in the pathogenesis of a variety of heart diseases.1 The acute production of excess ROS during ischemia–reperfusion injury triggers myocardial cell death. In addition, the continuous increase in ROS production and impaired energy production contribute to the development and progression of maladaptive cardiac remodeling and heart failure.2 Furthermore, lifelong exposure of mitochondria to oxidative stress leads to cardiac senescence. Thus, mitochondrion-protective antioxidants are powerful agents for the prevention and treatment of oxidative stress-associated heart diseases.