Figure 1.

Low-density lipoprotein (LDL) as the primary driver of atherogenesis. Key features of the influx and retention of LDL in the arterial intima, with ensuing pathways of modification leading to (i) extracellular cholesterol accumulation and (ii) formation of cholesteryl ester droplet-engorged macrophage foam cells with transformation to an inflammatory and prothrombotic phenotype. Both of these major pathways favour formation of the plaque necrotic core containing cellular and extracellular debris and LDL-cholesterol-derived cholesterol crystals. CE, cholesteryl ester; DAMPs, damage-associated molecular patterns; ECM, extracellular matrix; FC, free cholesterol; GAG, glycosaminoglycans; PG, proteoglycans; ROS, reactive oxygen species.