ABSTRACT
Atherosclerosis is the leading cause of morbidity and mortality among people with a Western lifestyle. The early atherosclerotic lesion is character-ized by the accumulation of arterial foam cells derived mainly from choles-terol-loaded macrophages (1, 2). Most of the accumulated cholesterol in foam cells originates from plasma low-density lipoprotein (LDL), which is inter-nalized into the cells via the LDL receptor. Native LDL, however, does not induce cellular cholesterol accumulation, because the LDL receptor activity is down regulated by the cellular cholesterol content (3, 4). LDL has to un-dergo some modifications, such as aggregation or oxidation, to be taken up by macrophages at enhanced rate via the macrophage scavenger receptors pathway, which, unlike the LDL receptor, are not subjected to downregulation by cellular cholesterol (57). The underlying mechanisms leading to the formation of atherosclerotic lesion are complicated and represent the outcome of multiple interactive processes (8-10).
