Moreover, oxidation can facilitate the disruption of high density lipid (HDL) functions, which ameliorate endothelial dysfunction, including activation of endothelial nitric oxide synthase (eNOS) leading to the increase of nitric oxide availability in the endothelial cells, endothelial repair, apoptosis, endothelial adhesion molecule/chemokine expression, and endothelial pro-thrombotic activation (31, 32). This evidence concerns the gene NOS3 and endothelial dysfunction.