Atherosclerosis Annotated Bibliography

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Inflammation in Atherosclerosis: From Pathophysiology to Practice Peter Libby, Paul M. Ridker, Göran K. Hansson, for the Leducq Transatlantic Network on Atherothrombosis J. Am. Coll. Cardiol. 2009;54;2129-2138 doi:10.1016/j.jacc.2009.09.009 This information is current as of February 22, 2011 The online version of this article, along with updated information and services, is located on the World Wide Web at: http://content.onlinejacc.org/cgi/content/full/54/23/2129 Downloaded from content.onlinejacc.org by on February 22, 2011 Journal of the American College of Cardiology © 2009 by the American College of Cardiology Foundation Published by Elsevier Inc. Vol. 54, No. 23, 2009 ISSN 0735-1097/09/$36.00 doi:10.1016/j.jacc.2009.09.009…show more content…
Knowledge has burgeoned regarding the operation of both innate and adaptive arms of immunity in atherogenesis, their interplay, and the balance of stimulatory and inhibitory pathways that regulate their participation in atheroma formation and complication. This revolution in our thinking about the pathophysiology of atherosclerosis has now begun to provide clinical insight and practical tools that may aid patient management. This review provides an update of the role of inflammation in atherogenesis and highlights how translation of these advances in basic science promises to change clinical practice. (J Am Coll Cardiol 2009;54:2129–38) © 2009 by the American College of Cardiology Foundation Just 3 decades ago the prevailing viewpoint envisaged atherosclerosis as a bland proliferative process (1). According to that concept, endothelial denuding injury led to platelet aggregation and release of platelet-derived growth factor that would…show more content…
These proinflammatory monocytes home to atherosclerotic lesions, where they propagate the innate immune response by expressing high levels of proinflammatory cytokines and other macrophage mediators, including matrix metalloproteinases (Fig. 1, left). Recent evidence has also highlighted the potential participation of mast cells in atherosclerosis. Long identified as a minority leukocyte population in the arterial adventitia and atherosclerotic intima, mast cells exhibit numerous functions implicated in atherogenesis (14,15). For example, mast cells release vasoactive small molecules such as histamine and leukotrienes, certain serine proteinases, and heparin, a cofactor in growth factor action and angiogenesis. Recent pharmacologic and genetic studies have provided firm evidence for mast cell participation in atherogenesis in mice (16,17). As established pharmacologic agents can modulate mast cell functions in humans, these recent observations also have therapeutic implications. The exten- Downloaded from content.onlinejacc.org by on February 22, 2011

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