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lüll Lecithin: cholesterol acyltransferase and atherosclerosis: another high-density lipoprotein story that doesn t quite follow the script Rader DJCirculation 2009[Aug]; 120 (7): 549-52Plasma concentrations of high-density lipoprotein cholesterol (HDL-C) are strongly, consistently, and independently inversely associated with risk of atherosclerotic cardiovascular disease (CVD). A series of animal studies in the 1990s, primarily involving overexpression of the major HDL protein apolipoprotein A-I (apoA-I) with subsequent increases in HDL-C, showed reduced progression or even regression of atherosclerosis, fitting nicely with the "HDL hypothesis" that raising HDL-C is causally associated with benefit. However, the last decade has seen several observations that do not follow this simple script. Some examples include the following: (1) the demonstration that scavenger receptor class BI knockout mice have increased HDL-C but increased atherosclerosis; (2) the suggestion that some persons with high HDL-C levels have "dysfunctional" HDL that may not be protective; and (3) the observation that the cholesteryl ester transfer protein inhibitor torcetrapib raised HDL-C levels considerably but did not decrease, and indeed increased, cardiovascular risk.(,) These developments have brought into major question the simple hypothesis that higher HDL-C directly and causally results in reduced atherosclerosis and challenge the approach of developing therapies that raise HDL-C levels.|Animals[MESH]|Atherosclerosis/epidemiology/*physiopathology[MESH]|Cholesterol, HDL/blood[MESH]|Disease Models, Animal[MESH]|Humans[MESH]|Lipoproteins, HDL/*physiology[MESH]|Mutation[MESH]|Phosphatidylcholine-Sterol O-Acyltransferase/genetics/*physiology[MESH]|Risk Factors[MESH] |