HTRA2 and myocardial infarction: These results not only support our previous study suggesting that cytoplasmic translocation of Omi/HtrA2 from the mitochondria promoted cardiomyocyte apoptosis after myocardial infarction (MI)9, a common translocational mechanism of Omi/HtrA2 induced apoptosis, but also yield mechanistic insight regarding how mitochondrial Omi/HtrA2 directly promotes myocardial apoptosis.