The risk of atherosclerosis has been known to be inversely correlated with the plasma concentration of high-density lipoprotein (HDL)-cholesterol, and we now know HDL plays a protective role against atherosclerosis. The most important mechanism, by which HDL could exert their anti-atherogenic role, is certainly the removal of excess cholesterol from peripheral cells and its transport to the liver, a process commonly called "reverse cholesterol transport system". In this system, many proteins are involved, i.e., ABC1, LCAT, CETP, HTGL and SR-BI. Abnormalities of these proteins reduce the efficacy of the system, and cause abnormalities of HDL and atherosclerosis. In this paper, we review the recent findings on the molecular mechanism of reverse cholesterol transport system, and then discuss hypo- and hyperalphalipoproteinemia, which are caused by genetic abnormalities of the key players.
|Number of pages||6|
|Journal||Nippon rinsho. Japanese journal of clinical medicine|
|Publication status||Published - 12-1999|
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