Monocytes in atherosclerosis: subsets and functions.
Chronic inflammation drives atherosclerosis, the leading cause of cardiovascular disease. Over the past two decades, data have emerged showing that immune cells are involved in the pathogenesis of atherosclerotic plaques. The accumulation and continued recruitment of leukocytes are associated with the development of 'vulnerable' plaques. These plaques are prone to rupture, leading to thrombosis, myocardial infarction or stroke, all of which are frequent causes of death. Plaque macrophages account for the majority of leukocytes in plaques, and are believed to differentiate from monocytes recruited from circulating blood. However, monocytes represent a heterogenous circulating population of cells. Experiments are needed to address whether monocyte recruitment to plaques and effector functions, such as the formation of foam cells, the production of nitric oxide and reactive oxygen species, and proteolysis are critical for the development and rupture of plaques, and thus for the pathophysiology of atherosclerosis, as well as elucidate the precise mechanisms involved.
Woollard
Kevin J
KJ
Center for Molecular and Cellular Biology of Inflammation (CMCBI), Division of Immunology, Infection and Inflammatory Diseases (DIIID), Guys Campus, London SE1 1UL, UK. kevin.woollard@kcl.ac.uk
Geissmann
Frederic
F
D000818:Animals; D050197:Atherosclerosis / Q000276:immunology* / Q000378:metabolism; D002454:Cell Differentiation; D002465:Cell Movement; D018450:Disease Progression; D006801:Humans; D007249:Inflammation / Q000276:immunology* / Q000378:metabolism; D018836:Inflammation Mediators / Q000378:metabolism; D008264:Macrophages / Q000276:immunology* / Q000378:metabolism; D009000:Monocytes / Q000276:immunology* / Q000378:metabolism; D012421:Rupture; D015398:Signal Transduction
D018836:Inflammation Mediators