On analysing the post-myocardial infarction (MI) phase, animal studies have shown that BDNF plasma levels are significantly higher in mice with myocardial ischemia, and BDNF expression is upregulated by neural signals from the heart after MI to protect the myocardium from ischemic damage: BDNF/TrkB indeed attenuates ischemic heart damage and inhibits cardiomyocyte apoptosis by regulating TRPC3/6 channels [60,64,65]. Here, TRPC3 is linked to myocardial infarction.