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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.