Inflammation in atherosclerosis.
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.
Libby
Peter
P
Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. plibby@rics.bwh.harvard.edu
D000818:Animals; D001161:Arteriosclerosis / Q000209:etiology* / Q000276:immunology / Q000473:pathology* / Q000628:therapy; D002634:Chemotaxis, Leukocyte; D004198:Disease Susceptibility; D006801:Humans; D007249:Inflammation / Q000150:complications* / Q000276:immunology / Q000473:pathology / Q000628:therapy; D007962:Leukocytes / Q000276:immunology; D012306:Risk; D017539:Tunica Intima / Q000276:immunology / Q000473:pathology