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- W2118127418 abstract "See related article, pages 792–801 The deleterious effects of high low-density lipoprotein (LDL) cholesterol levels on atherosclerosis has been known for almost a century,1 yet plasma cholesterol continues to be a challenge for clinicians in the treatment and prevention of cardiovascular disease.2,3 Atherogenesis involves uptake of cholesterol in the vascular wall, followed by inflammatory activation and growth of vascular smooth muscle cells.4,5 Indeed, proinflammatory mediators such as interleukins and cytokines stimulate vascular cell growth and atherogenesis (reviewed in4), whereas inhibition of inflammatory pathways attenuates cell growth and atherosclerosis.6 Therefore, we now view atherosclerosis as a vascular inflammatory process7 as was already proposed by Virchow8 and later by Anitschkow who noticed an “infiltrative character” of atherosclerotic lesions of cholesterol-fed animals.9Differentiation and growth of vascular smooth muscle cells, a prerequisite of atherosclerosis progression, depends on a fine-tuned balance between activators and inhibitors of cell growth.10 In the 1980s, Libby and colleagues reported that LDL cholesterol enhances growth factor–stimulated proliferation of …" @default.
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- W2118127418 date "2007-10-12" @default.
- W2118127418 modified "2023-09-23" @default.
- W2118127418 title "Inflammation and Atherosclerosis" @default.
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- W2118127418 doi "https://doi.org/10.1161/circresaha.107.162487" @default.
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