High-density lipoproteins (HDL) are believed to protect against athero
sclerosis by promoting the process of reverse cholesterol transport. T
his process involves different steps including efflux of cellular chol
esterol, cholesterol esterification and lipid transport and exchange.
Apolipoprotein-(apo) A-I, the major HDL apolipoprotein, and the HDL-as
sociated enzyme lecithin-cholesterol acyltransferase (LCAT), which use
s apo A-I as a cofactor play a crucial role in reverse cholesterol tra
nsport. HDL may he classified into species according to their apolipop
rotein content. Recent data concerning HDL particles indicate that lip
oproteins containing apo A-I but not ape A-II (LpA-I) are more effecti
ve carriers of free cholesterol and are associated with a protective e
ffect agains coronary heart disease. In vitro studies have shown that
glycosylated HDL are functionally abnormal and may be considered ather
ogenic. Our study considers the different impacts of non-enzymatic gly
cosylation of ape A-I or protein-HDL on the reverse cholesterol transp
ort process.