Abstract
Lecithin cholesterol acyltransferase (LCAT) is a key enzyme that catalyzes the esterification of free cholesterol in plasma lipoproteins and plays a critical role in high density lipoprotein (HDL) metabolism. LCAT deficiency leads to accumulation of nascent pre-HDL due to impaired maturation of HDL particles, whereas enhanced expression is associated with the formation of large, apoE-rich HDL 1 particles. In addition to its function in HDL metabolism, LCAT was believed to be an important driving force behind macrophage reverse cholesterol transport (RCT) and, therefore, has been a subject of great interest in cardiovascular research since its discovery in 1962. Although half a century has passed, the importance of LCAT for atheroprotection is still under intense debate.
Highlights
Lecithin cholesterol acyltransferase (LCAT) STRUCTURE AND FUNCTION The human LCAT primarily produced by the liver, it is expressed in small amounts by intestine and in astrocytes in the brain, where it is involved in the cholesterol esterification in glia-derived apoE-containing lipoproteins [20, 24, 39, 41]
It appears that the influence of LCAT on atherosclerosis mostly depends on its effects on proatherogenic apoB-containing lipoproteins
Viral overexpression of LCAT in nonhuman primates resulted in an antiatherogenic profile characterized by decreased levels of apoB-containing lipoproteins and increased level of high density lipoprotein (HDL) cholesterol [3], similar to that observed in the transgenic rabbits
Summary
The human LCAT primarily produced by the liver, it is expressed in small amounts by intestine and in astrocytes in the brain, where it is involved in the cholesterol esterification in glia-derived apoE-containing lipoproteins [20, 24, 39, 41]. The human LCAT half-life in plasma has been estimated to be 4-5 days [36] ApoAI is the most potent activator of LCAT, which enables it to synthesize cholesteryl esters from the free cholesterol on HDL by a transesterification reaction involving the transfer of a fatty acid at the sn -2 position of lecithin to the free hydroxyl group of cholesterol [14, 24]. During this reaction, lecithins are converted into lysophosphatidylcholines. In addition to its essential role in the first step of the RCT pathway, LCAT enhances the delivery of cholesterol to the liver [16]
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