Abstract
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.
Key Points
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Atherosclerosis has long been associated with chronic inflammation
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The accumulation of macrophages correlates with atherosclerotic plaque progression and plaque rupture
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Monocytes accumulate at sites of inflammation and have been reported to enter atherosclerotic plaques
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Macrophages and foam cell are present in plaques and might derive from monocytes or from resident macrophages
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Monocytes represent a heterogeneous population of cells with differences in phenotype, function and locomotion
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Acknowledgements
K. J. Woollard is funded by a British Heart Foundation fellowship. Work in F. Geissmann's lab is supported by the Arthritis Research Campaign and the Medical Research Council (G0900867 Strategic Award).
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Woollard, K., Geissmann, F. Monocytes in atherosclerosis: subsets and functions. Nat Rev Cardiol 7, 77–86 (2010). https://doi.org/10.1038/nrcardio.2009.228
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DOI: https://doi.org/10.1038/nrcardio.2009.228