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Figure 2 Proposed Biochemical and Cellular Mechanisms of Enhanced Small, Dense LDL

Increased small dense low-density lipoprotein (LDL) production, combined with a lower affinity of small, dense LDL for the low-density lipoprotein receptor (LDL-R) and a longer residence time in plasma, leads to an increased number of small, dense LDL particles. The increased small, dense LDL cross the arterial wall more readily, bind more avidly to proteoglycans in the intimal matrix, and are more easily oxidized, characteristics all conducive to atherogenesis (16). Small, dense LDL promotes endothelial cell dysfunction, inducing greater production of plasminogen activator inhibitor (PAI)-I and thromboxane A₂ (TXA₂).