Figure 1. Summary of the role of Ox-LDL in atherosclerosis progression. Ox-LDL promotes atherosclerotic events right from their initiation 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. 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 in a rupture-prone thrombus. Adapted from Khatana et al. (2020).
