LOX and myocardial infarction: In summary, this study demonstrates that although LOX transgenesis boosts cardiac oxidative stress under basal conditions, LOX over-expression in mice does not result in exacerbated ROS production or altered infarct size and functional recovery in response to acute myocardial ischemia-reperfusion injury, and does not modify post-myocardial infarction remodeling triggered by transient coronary occlusion, a model resembling the clinical scenario of patients with STEMI subjected to PCI.