NTRK1 and myocardial infarction: Therefore, we speculated that LXFG may be regulating expression of effector P-Bad via the NGF/TrKA/PI3K/AKT signaling pathway, causing a balance between survival, regeneration, and apoptosis of sympathetic neurons, thereby attenuating sympathetic remodeling and reducing occurrence of arrhythmia in rats following MI.