CAMK2G and myocardial infarction: Here, we identify increased mitochondrial CaMKII activation in failing mouse hearts 1 week after myocardial infarction surgery, and find that mouse hearts with myocardial and mitochondrial CaMKII inhibition, due to transgenic expression of a potent, and selective CaMKII inhibitor polypeptide (mtCaMKIIN)25, are protected from left ventricular dilation and dysfunction 1 week after myocardial infarction.