UCP2 and myocardial infarction: These data suggest that ucp3 deletion might exert detrimental effects on cardiac function and remodeling of the ischemic heart via other mechanisms, eventually acting in surviving cells, including vascular rarefaction.25,49 Importantly, MI hearts from ucp3−/− mice were characterized by structural and functional mitochondrial abnormalities and increased mitochondrial ROS production despite a normal induction of ucp2 mRNA/protein levels in vitro and in vivo (Figure 9A through 9F).