The sub-endothelial retention of lipoproteins is one of the key events that trigger the atherosclerosis process. Low-density lipoprotein (LDL) particles trapped within the arterial wall are prone to progressive oxidation by monocytes/macrophages. Oxidized LDL (oxLDL) is present in atherosclerotic lesions, and has been suggested to play a significant role in atherogenesis. The pathophysiology of atherosclerosis involves both apoptosis and proliferation at different stages of the vessel lesion. In advanced atherosclerotic plaques, up to 50% of the apoptotic cells are macrophages, which may promote core expansion and plaque instability.
In our study, we defined the mechanism by which oxLDL induces apoptotic cell death in the J774A.1 macrophage cell line, a widely used in vitro model for evaluating the mechanisms underlying the adverse effects of oxidized lipids and oxLDL with native LDL (nLDL) as the control.