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Inflammation in atherosclerosis

Abstract

Abundant data link hypercholesterolaemia to atherogenesis. However, only recently have we appreciated that inflammatory mechanisms couple dyslipidaemia to atheroma formation. Leukocyte recruitment and expression of pro-inflammatory cytokines characterize early atherogenesis, and malfunction of inflammatory mediators mutes atheroma formation in mice. Moreover, inflammatory pathways promote thrombosis, a late and dreaded complication of atherosclerosis responsible for myocardial infarctions and most strokes. The new appreciation of the role of inflammation in atherosclerosis provides a mechanistic framework for understanding the clinical benefits of lipid-lowering therapies. Identifying the triggers for inflammation and unravelling the details of inflammatory pathways may eventually furnish new therapeutic targets.

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Figure 1: Mononuclear phagocytes in atherogenesis.
Figure 2: The roles of T lymphocytes in atherogenesis.
Figure 3: Recruitment and functions of mast cells in atherogenesis.
Figure 4: Schematic of the life history of an atheroma.

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Libby, P. Inflammation in atherosclerosis. Nature 420, 868–874 (2002). https://doi.org/10.1038/nature01323

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