DNM1L and myocardial infarction: In apparent support of this concept, pre-ischemic administration of the agents MDIVI-1 (mitochondrial division inhibitor-1: the putative archetypal small molecule inhibitor of DRP1), P110 and Dynasore, as well as siRNA-mediated knockdown of DRP1 and transfection with a dominant negative DRP1 mutant, have all been show to attenuate mitochondrial fragmentation, improve cardiomyocyte viability in cell culture models of IR, and reduce infarct volumes in in vivo models of acute MI [23,24,26,28,123,184,185].