Atherosclerosis: cell biology and lipoproteins focus on epigenetic modification and macrophage biology

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Cardiovascular diseases (CVDs) are the leading cause of mortality worldwide, with millions of deaths annually. The main cause of CVD is atherosclerosis, a gradually progressing, chronic inflammatory disorder of the arteries eventually precipitating severe clinical manifestations such as myocardial infarction or stroke. The disease is driven by the accumulation of lipids and a variety of inflammatory cells in the arterial wall, hence hypercholesterolemia and the immune system are major propagators of atherosclerosis [1]. A decade ago, seminal work by Swirski et al.[2] described an inherent connection of persistent hypercholesterolemia and systemically increased levels of Ly6Chi monocytes in experimental models of atherosclerosis. Since, a number of studies have addressed the phenotype and transition of monocytes and macrophages in the field of atherosclerosis [3].

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