High amounts of oxLDL lead to an imbalance of eNOS and iNOS mediated by High-mobility group box 1 (HMGB1)-toll-like receptor (TLR) pathway and lectin-type oxLDL receptor 1 (LOX-1)-nuclear factor-κB (NF-κB) pathway respectively, ultimately resulting in endothelial dysfunction due to EC apoptosis and reduced protective autophagy [64]. Here, NOS3 is linked to endothelial dysfunction.