Atherogenic lipoproteins such as LDL enter macrophages within the blood vessel wall and promote the growth of an atherosclerotic plaque. HDL in the plasma is antiatherogenic and removes cholesterol from the macrophages, preventing the growth or even regression of the atherosclerotic plaque. Aggressive targeting of lipids on both sides of this equation, both the LDL and the HDL, is likely to be maximally effective in reducing cardiovascular risk.The passage of HDL cholesterol back to the liver is not without interruption. HDL particles interact with both LDLs and VLDLs, and in so doing they exchange cholesterol for triglyceride via the actions of a protein called cholesterol ester transfer protein and the enzyme lecithin-cholesterol acyltransferase (LCAT).
Cholesterol ester transport protein depletes HDL of cholesterol while concomitantly increasing the amount of cholesterol in the outward-going VLDL and LDL particles. At first glance, it may seem disadvantageous for cholesterol to remain in the atherogenic LDL and VLDL fractions of the lipoproteins. However, the mechanism scavenges cholesterol from the periphery, thus relieving cells of the metabolically expensive process of de novo synthesis.