Activation of Notch signaling reduces myocardial ischemia reperfusion injury (MI/RI), by activating key components of survival pathways, namely, PI3K-Akt, NOS, and mitochondrial K+-ATP (mitoKATP) channels [231]; BBR, polydatin, and 2,3,5,4′-tetrahydroxystilbene-2-O-β-D-glucoside upregulate Notch-1/HES1 signaling attenuating myocardial apoptosis both in cultured cardiomyocytes and in rats subjected to MI/RI [304–306]. This evidence concerns the gene NOTCH1 and myocardial infarction.