Further, increased vascular permeability due to hyperglycemia leads to leukocyte infiltration of the cardiac interstitium, DAMPs signaling by mitochondrial stress via lipotoxicity, and cardiomyocyte apoptosis induce activation of TLR2 and TLR4 along with increased NLRP3, driving the pro-caspase-1 recruitment for inflammasome formation, amplifying myocardial cytokine production, macrophage infiltration, and cardiomyocyte apoptosis and peripheral cardiac fibrosis [26,29,30,31]. This evidence concerns the gene TLR2 and Hyperglycemia.