Lecithin–cholesterol acyltransferase (LCAT)

Lecithin–cholesterol acyltransferase (LCAT) is a plasma enzyme primarily associated with high-density lipoprotein (HDL) particles, responsible for catalyzing the esterification of free cholesterol with the sn-2 position of phosphatidylcholine (lecithin), forming cholesteryl esters and lysophosphatidylcholine[1][2][6][9]. This reaction is a critical step in the reverse cholesterol transport pathway, facilitating the removal of excess cholesterol from peripheral tissues to the liver for excretion. LCAT is activated by apolipoprotein A-I (ApoA-I) in HDL, and its deficiency leads to abnormal lipid metabolism, resulting in disorders such as familial LCAT deficiency and fish-eye disease[1][2][4][5][7][9]. Therapeutic strategies involving recombinant LCAT or enzyme activators are under investigation for cardiovascular and renal diseases as well as rare lipid disorders, although the ultimate protective role of LCAT in atherosclerosis remains debated[4][5].

Other names

phosphatidylcholine–sterol O-acyltransferasephosphatidylcholine-sterol acyltransferase

Cholesterol esterification: Transfers an acyl group from phosphatidylcholine (lecithin) to free cholesterol, forming cholesteryl esters and lysophosphatidylcholine[1][2][6][7][9]. Drugs: Recombinant LCAT directly replaces enzyme activity; small molecule activators increase endogenous LCAT activity.