Taken together, these findings highlight a dual axis, whereby NGF-TRPV1 signaling preserves microvascular integrity and limits I/R injury in diabetic hearts, while therapies such as DPP-4 inhibition can modulate NGF-driven sympathetic remodeling through redox-sensitive HO-1 pathways, offering novel diagnostic and therapeutic avenues for DCM [79] (Figure 2). This evidence concerns the gene DPP4 and familial dilated cardiomyopathy.