Retention of atherogenic lipoproteins in the artery wall and its role in atherogenesis

Proteoglycan structures and the proteoglycan interaction with low-density lipoproteins (LDL). A) The most common proteoglycan species in the arterial wall. B) The LDL-proteoglycan interaction. Clusters of positively charged amino acids on apolipoprotein B (apoB) bind to negatively charged glycosaminoglycan (GAG) chains on proteoglycans.

The response-to-retention hypothesis of atherosclerosis. Areas with diffuse intimal thickening contain high quantities of proteoglycans that capture lipoproteins. The retained lipoproteins trigger an inflammatory response, which in turn further increases the lipoprotein retention by the release of bridging molecules and the stimulation of proteoglycan production. Consequently, lipoprotein retention is part of a vicious circle that ultimately leads to a maladapted inflammation and atherosclerosis.