NTRK2 and myocardial infarction: In support of this hypothesis, the pathological phenotypes seen in this study and the report using an inducible 2-month-old cardiomyocyte-specific TrkB conditional knockout MI mouse model (blockade of cardiomyocyte and non-cardiomyocyte-derived BDNF signaling), which included decreased cardiac function and myocardial angiogenesis in the infarct border zone and increased infarct size and cardiomyocyte apoptosis (22), clearly suggest that in the adult heart, cardiomyocyte-derived BDNF is irreplaceable for maintaining the integrity of cardiac pathophysiology and regenerating injured myocardium.