Is reverse cholesterol transport a misnomer for suggesting its role in the prevention of atheroma formation? Review Article

Reverse cholesterol transport from peripheral tissues, including the arterial wall, involves high density lipoprotein (HDL) uptake of unesterified cell cholesterol, its esterification by lecithin-cholesterol-acyl-transferase (LCAT), direct HDL-cholesteryl ester uptake by the liver and the indirect pathway consisting of the cholesteryl ester transfer protein (CETP)-mediated transfer of HDL-cholesteryl ester to apolipoprotein (apo) B-containing lipoproteins (very low density lipoprotein (VLDL) and LDL). Although the first route should be regarded as anti-atherogenic, ambiguous interpretations are drawn from the indirect pathway since it is potentially atherogenic to the extent that it may raise the plasma cholesteryl ester concentration in lipoproteins that are taken up by arterial wall macrophages. In addition, controversial roles are played in reverse cholesterol transport by LCAT and liver uptake of HDL-cholesteryl ester mediated by hepatic lipase (HL). HDL may exert several antiatherogenic effects unrelated to its role in cell cholesterol removal.