Key result
LCAT deficiency significantly reduced aortic atherosclerosis (-35% to -99%) in all mouse models despite decreased HDL cholesterol levels.
Why the study?
Does LCAT deficiency affect the development of glomerulosclerosis and atherosclerosis in mouse models?
Population
LCAT knockout mice cross-bred with apolipoprotein E KO, low density lipoprotein receptor KO, and cholesteryl…
Comparison
LCAT gene knockout (LCAT deficiency) vs Control mice without LCAT deficiency
Design
Preclinical
Authors
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Questions HDL as primary atherosclerosis driver in LCAT-deficient mice; leaves open human relevance and non-HDL mechanisms.
Does LCAT deficiency affect the development of glomerulosclerosis and atherosclerosis in mouse models?
Effect estimate: -35% to -99%
In mouse models, LCAT deficiency reduces atherosclerosis despite lowering HDL cholesterol, suggesting that concurrent reductions in non-HDL cholesterol drive the atheroprotective effect.
Lambert et al. (2001) studied Familial lecithin cholesterol acyl transferase (LCAT) deficiency. LCAT deficiency (LCAT knockout) vs. Control mice was evaluated on Aortic atherosclerosis (-35% to -99%). LCAT deficiency significantly reduced aortic atherosclerosis (-35% to -99%) in all mouse models despite decreased HDL cholesterol levels.
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