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Inflammation in atherosclerosis

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  • Peter Libby

    (Brigham and Women's Hospital, and Harvard Medical School)

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.

Suggested Citation

  • Peter Libby, 2002. "Inflammation in atherosclerosis," Nature, Nature, vol. 420(6917), pages 868-874, December.
    • Handle: RePEc:nat:nature:v:420:y:2002:i:6917:d:10.1038_nature01323
    DOI: 10.1038/nature01323
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