Mechanistic Insights into the Oxidized Low-Density Lipoprotein-Induced Atherosclerosis

Figure 6

Schematic illustration of the role of Ox-LDL in atherosclerosis progression. Ox-LDL elicits atherosclerotic events right from their production in the subendothelium. Due to downregulated LDL receptors, the native LDL cannot be internalized by macrophages. Ox-LDL, via LOX 1 and other factors, activates endothelium for a number of events: adherence of LDL, monocytes, and platelets; secretion of chemokines and growth factors; production of ROS; impairing NO secretion; and so on. SRs, CD36, and LOX 1 help in the uptake of OX-LDL by monocyte-derived macrophages in the subendothelium. Growth factors mediate SMC proliferation and extracellular matrix formation. Platelet adherence and accumulation is also, in part elicited by Ox-LDL which results into a rupture prone thrombus.