*Geek Box: Atherogenicity of LDL Particles
LDL particles pass through the arterial endothelium and enter the arterial intima, where the apolipoprotein B [ApoB] protein binds with proteoglycans in the arterial intima. This results in those ApoB-expressing LDL particles being retained in the arterial intima, where they accumulate, and the retention of LDL in the artery is the fundamental step in atherosclerosis.
Certain characteristics of LDL particles may increase the atherogenicity of the particles that have been retained, including the factors listed in the figure, above. Following retention by ApoB binding to intimal proteoglycans, LDL particles undergo modification processes that trigger the development of atherosclerotic lesions in the artery.
For example, the environment within the intima renders LDL particles prone to oxidation, and oxidised LDL generates an inflammatory and immune system response that recruits macrophage immune cells to the arterial wall. Macrophages uptake oxidised LDL resulting in the generation of cholesterol-rich foam cells.
Several LDL particles may also aggregate together through contact between their cell surfaces, attaching these particles together which promotes their uptake by macrophages. Aggregated LDL particles may also fuse together to form a larger particle. The process of LDL aggregation is potentially reversible, including through diet, but the fusing of LDL is irreversible.