Figure 1.

Apolipoprotein A-1 (ApoA-1) is synthesized in the liver and the intestine and secreted in a lipid-free state. Assembly of the HDL particle begins with the lipidation of the ApoA-1 protein via ABCA-1 cholesterol efflux, creating a discoidal shape termed pre-β HDL. Lipidation of pre-β HDL via LCAT results in the formation of small, spherical HDL particles. Further re-modelling of the HDL particle is a complex metabolic process that involves several enzymes. The HDL particles may grow in size by accumulating cholesterol and other lipids from peripheral tissue, a process termed reverse cholesterol transport (RCT), widely considered to be the main function of HDL. HDLs may shrink in size by delivery of cholesterol and lipids to steroidogenic tissue via Scavenger Receptor-B1 (SR-B1), peripheral tissue and the liver via endothelial (EL) and hepatic lipases (HL), or lipid exchange via CETP to apoB-containing lipoproteins. After a 4-to-5-day life cycle HDLs are permanently catabolized in the liver or kidneys.