Reverse Cholesterol Transport and Atherosclerosis Regression

holesterol is the major component of atherosclerotic plaque.Cholesterol accumulation within atherosclerotic plaque occurs when cholesterol influx into the arterial wall (from apoB-containing lipoproteins) exceeds cholesterol efflux.Increased influx of cholesterol into the arterial wall is accompanied by an increased influx of monocytes/macrophages, 1 which take up oxidized and aggregated LDL and store the cholesterol as esters.Whereas parenchymal cells maintain cholesterol balance by downregulating de novo cholesterol synthesis and LDL receptor expression, macrophages continue to take up cholesterol from apoB-containing lipoproteins via pathways that are not subject to sterol-mediated feedback control.Current strategies to reduce coronary heart disease (CHD) are aimed primarily at reducing the influx of cholesterol into the arterial wall by lowering plasma LDL cholesterol concentrations.Aggressive lowering of plasma LDL levels reduces mortality from CHD, 2 but protection is not complete, and in a significant proportion of patients, plasma LDL concentrations cannot be lowered to a level that would be predicted to halt the progression of disease.As a consequence, there is great interest in strategies aimed at enhancing cholesterol efflux from the arterial wall and promoting its transport to the liver for excretion.