Figure 1

Simplified scheme of reverse cholesterol transport. In the onset and progression of atherosclerotic lesions the uptake of modified LDL (mainly oxidized LDL or oxLDL) by macrophages through a process mediated by scavenger receptors (i.e. SR-A and CD36) that lead to the formation of lipid-loaded cells is critical. This seems to be a reversible process, as HDL-mediated RCT can clear cholesterol from vascular tissues contributing to atherosclerosis regression. HDL acquires cholesterol through a mechanism that involves the receptor SR-BI and transports this cholesterol back to the liver. However, HDL also exchanges lipids with LDL, a process mediated by the CETP that increases LDL cholesterol cargo and potentially enhances their atherogenicity.