Inflammation in atherosclerosis
Peter Libby ()
Additional contact information
Peter Libby: Brigham and Women's Hospital, and Harvard Medical School
Nature, 2002, vol. 420, issue 6917, 868-874
Abstract:
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.
Date: 2002
References: Add references at CitEc
Citations: View citations in EconPapers (40)
Downloads: (external link)
https://www.nature.com/articles/nature01323 Abstract (text/html)
Access to the full text of the articles in this series is restricted.
Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.
Export reference: BibTeX
RIS (EndNote, ProCite, RefMan)
HTML/Text
Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:420:y:2002:i:6917:d:10.1038_nature01323
Ordering information: This journal article can be ordered from
https://www.nature.com/
DOI: 10.1038/nature01323
Access Statistics for this article
Nature is currently edited by Magdalena Skipper
More articles in Nature from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().