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Atherosclerosis is an inflammatory vascular disorder. Population studies linked hypercholesterolemia with coronary risk several decades ago. In the 1990s, preclinical and clinical evidence on lowering low-density lipoprotein (LDL) established that cholesterol not only promotes atherogenesis but also triggers the onset of acute thrombotic complications. Hypercholesterolemia promotes endothelial cell activation, recruiting circulating monocytes into the arterial wall, where they differentiate into macrophages. These proinflammatory phagocytes then become lipid-laden foam cells, a hallmark of atherosclerosis.1–3 Although the direct role of loaded lipids remains obscure, these activated macrophage foam cells (as gauged by the expression of high levels of proinflammatory factors such as cytokines and chemokines) activate vascular smooth muscle cells (SMCs), endothelial cells, and neighboring macrophages and induce the infiltration of additional immune cells into the lesion, which amplifies the atherogenic milieu in arteries. Matrix-degrading enzymes released by foam cells, such as matrix metalloproteinases (MMPs), and thrombogenic factors (eg, tissue factor) may reduce the mechanical stability of atherosclerotic plaques and trigger acute thrombosis.4 A global proteomic analysis by Becker et al5 in control and cholesterol-loaded macrophages identified 46 proteins that respond to sterol loading of macrophages in vivo. These proteins participate in lipid binding, cytoskeletal regulation, and vesicle-mediated transport and are enriched in factors associated with causative roles in atherogenesis.5Article see p 1209The underlying mechanisms for foam cell formation remained obscure until the 1980s.6 Joseph L. Goldstein and Michael S. Brown reported that although the incubation of macrophages in culture with native LDL did not substantially cause foam cell formation, the cells rapidly took up chemically modified LDL (acetyl LDL) and became foamy cells, which led to the discovery of the acetyl LDL receptor by the same group and the subsequent cloning of the scavenger receptor A-I by Monty Krieger and Tatsuhiko Kodama. …

Liver-Artery Interactions via the Plasminogen-CD36 Axis in Macrophage Foam Cell Formation