ated upon LDL retention by the arterial proteoglycans and LDL modifi cation by the resident hydrolases and oxidative agents ( 1-3 ). These modifi cations trigger a cascade of pro-infl ammatory and pro-apoptotic responses that are caused, in part, by the toxic effects of the oxidized phospholipids and their hydrolytic products such as FFA and lyso-phosphatidylcholine (PC) ( 4, 5 ). Hydrolytic and oxidative modifi cations can also induce LDL aggregation, fusion, and coalescence into lipid droplets, which further enhance LDL retention in the arterial wall ( 6 ). LDLderived small extracellular lipid droplets (30-400 nm) are prominent in early atherosclerotic lesions ( 7 ) and are observed in the experimental models of atherosclerosis [( 8 ) and references therein]. Most of the lipids found in fibrous atherosclerotic plaques are present in such droplets [reviewed in ( 9 )]. Moreover, fusion of modifi ed LDL accelerates LDL uptake by arterial macrophages, eventually leading to foam cell formation and progression of atherosclerotic plaques containing large (400-6,000 nm) LDL-derived intracellular lipid droplets ( 7 ). Hence, the atherogenic potential of LDL is linked to their propensity to fuse and coalesce into lipid droplets.Because nonmodifi ed LDL do not fuse under physiologic conditions, modifi cations such as oxidation, lipolysis, and proteolysis are thought to be prerequisites for lipoprotein fusion [( 1-4, 10 ) and references therein]. The effects of these modifi cations on LDL aggregation and fusion have been attributed to the packing defects in the particle surface ( 6, 8 ), which may result from an imbalance between this surface and the apolar core ( 12 ). A similar imbalance leading to lipoprotein fusion and rupture can result from other perturbations such as heating, chemical In atherosclerosis, LDL-derived lipids are deposited in the subendothelium of the arterial wall. According to the "response to retention" hypothesis, atherogenesis is initi-