Moreover, the overexpression of a dominant-negative Nox4 mutant resulted in reductive stress and increased mitochondrial ROS, infarction size, and myocardial energetic deficits in response to ischemia-reperfusion injury [102], suggesting that NOX4 also has adaptive functions in modulating inflammation and injury resolution in the ischemic myocardium. Here, NOX4 is linked to infarction.