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(Circulation. 2007;115:2471-2473.)
© 2007 American Heart Association, Inc.

Editorial

Mast Cells as Mediators and Modulators of Atherogenesis

Peter Libby, MD; Guo-Ping Shi, DSc

From the Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass.

Correspondence to Peter Libby, MD, Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115. E-mail plibby@rics.bwh.harvard.edu

Key Words: Editorials • atherosclerosis • leukocytes • inflammation

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
The central role of inflammation in atherogenesis has gained broad acceptance and has revolutionized our understanding of this common disease. This recognition has heightened interest in identifying the specific mediators and mechanisms that contribute to the interplay between risk factors (traditional and emerging), inflammation, and the altered biology of the arterial wall that regulates plaque development and complication.¹ In particular, leukocytes have come to occupy center stage as the major cellular effectors of inflammation. When these inflammatory cells join endothelial and smooth-muscle cells in the artery wall, they spur much of the biology that drives atherogenesis and plaque complication.

Article p 2516

The list of leukocyte subtypes involved in arterial inflammation has entered a flourishing phase of refinement. Our understanding of leukocyte involvement in atherogenesis has gone through several strata of discovery and probing. During the initial descriptive phase, the use of rigorous molecular markers buttressed venerable morphological observations and verified the presence of various leukocyte classes within lesions.² Later, a phase of experimental validation established the causal relationship between leukocyte accumulation in lesions and the aspects of atherogenesis.^3–5 Next, continuing mechanistic exploration has probed the precise molecular pathways by which a given leukocyte population can promote or otherwise modify disease.⁶ Ultimately, the human relevance of in vitro and animal experiments requires observations in human tissues and in patients.

	First Monocyte/Macrophages...

 
The saga of the macrophage in atherosclerosis followed this pattern. Initial morphological observations supported an early role of monocyte recruitment in the formation of experimental atherosclerotic lesions in rabbits—observations that extend . . . [Full Text of this Article]

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