Hepatic lipase (HL) plays a key role in the metabolism of proatherogenic and antiatherogenic lipoproteins by affecting their plasma level and physicochemical properties. Despite recent advances in the understanding of HL function in lipoprotein metabolism, its local involvement in atherosclerosis has been unclear. In the August 1 Journal of Clinical Investigation, Zengxuan Nong and colleagues at the National Heart, Lung, and Blood Institute show that macrophage-derived HL contributes directly, through a novel mechanism, to early aortic lesion formation in mice (Journal of Clinical Investigation, 112:367-378, August 1, 2003).

Nong et al. used apolipoprotein E–knockout (apoE-KO) and apoE-KO × HL-KO mice, and lecithin cholesterol acyltransferase–Tg (LCAT-Tg) and LCAT-Tg × HL-KO mice, which have a reduced aortic atherosclerosis potential. They observed that donor macrophages expressed HL in the artery wall and enhanced early aortic lesion formation in both apoE-KO and LCAT-Tg mice. However, expression of HL by macrophages did...

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