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.
Keywords
AtheromaInflammationInflammatory responseMedicineMacrophageThrombosisDownregulation and upregulationImmunologyBioinformaticsBiologyCardiologyInternal medicine
MeSH Terms
AnimalsArteriosclerosisChemotaxisLeukocyteDisease SusceptibilityHumansInflammationLeukocytesRiskTunica Intima
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Publication Info
- Year
- 2002
- Type
- review
- Volume
- 420
- Issue
- 6917
- Pages
- 868-874
- Citations
- 8008
- Access
- Closed
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Cite This
Peter Libby
(2002).
Inflammation in atherosclerosis.
Nature
, 420
(6917)
, 868-874.
https://doi.org/10.1038/nature01323
Identifiers
- DOI
- 10.1038/nature01323
- PMID
- 12490960