Figure 1. Lipoprotein modulation of atherosclerosis, beyond LDL.

Circulating lipoproteins other than LDL modulate the development of atherosclerosis. Animal and human data show that cholesteryl ester–rich lipoproteins derived from the partial catabolism of TRLs, referred to as remnants, are taken up by macrophage foam cells in arteries, promoting development of atherosclerotic plaques. The catabolism of TRLs also mediates enrichment of HDL with phospholipids, increasing their ability to promote efflux of cholesterol from foam cells and thus ameliorating atherosclerosis. The interchange of lipids between HDL and TRL is mediated by cholesteryl ester transfer protein (CETP) and phospholipid transfer protein (not shown). CE, cholesteryl ester; LPL, lipoprotein lipase; PL, phospholipids.