Inflammation in atherosclerosis.
Experimental work has elucidated molecular and cellular pathways of inflammation that promote atherosclerosis. Unraveling the roles of cytokines as inflammatory messengers provided a mechanism whereby risk factors for atherosclerosis can alter arterial biology, and produce a systemic milieu that favors atherothrombotic events. The discovery of the immune basis of allograft arteriosclerosis demonstrated that inflammation per se can drive arterial hyperplasia, even in the absence of traditional risk factors. Inflammation regulates aspects of plaque biology that trigger the thrombotic complications of atherosclerosis. Translation of these discoveries to humans has enabled both novel mechanistic insights and practical clinical advances.
Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA. plibby@rics.bwh.harvard.edu
Peter
P
Libby
D056704:Adaptive Immunity; D000818:Animals; D001158:Arteries / Q000276:immunology* / Q000473:pathology; D050197:Atherosclerosis / Q000276:immunology* / Q000473:pathology; D016207:Cytokines / Q000378:metabolism; D006084:Graft Rejection / Q000276:immunology / Q000473:pathology; D006801:Humans; D006965:Hyperplasia; D007113:Immunity, Innate; D007249:Inflammation / Q000276:immunology* / Q000473:pathology; D018836:Inflammation Mediators / Q000378:metabolism*; D008264:Macrophages / Q000276:immunology; D058226:Plaque, Atherosclerotic; D015398:Signal Transduction
D016207:Cytokines; D018836:Inflammation Mediators