doi: 10.1161/01.RES.0000223519.26857.5d
© 2006 American Heart Association, Inc.
Editorials |
A Farewell Kiss Triggers a Broken Heart?
From the Heart and Lung Research Institute, Ohio State University, Columbus.
Correspondence to Nicholas A. Flavahan, The Ohio State University, 473 West 12th Ave, R 110E, Columbus, OH 43210. E-mail nicholas.flavahan@osumc.edu
See related article, pages 1168–1176
Key Words: vascular smooth muscle • apoptosis • atherosclerosis • T cells • CD4
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
The evolving atherosclerotic lesion reflects a coordinated interaction between vascular and immune/inflammatory cells.1,2 Foam cells and extracellular lipid droplets form the central core of the atheroma, which is covered by vascular smooth muscle cells (VSMCs) and a collagen-rich matrix. T cells and macrophages infiltrate the lesion and are particularly abundant in the shoulder region. VSMCs are responsible for producing extracellular matrix proteins that provide strength and stability to the lesion. Indeed, the atherosclerotic plaque can remain relatively stable in which a cap of VSMCs and matrix proteins covers the lipid core. Alternatively, the plaque can develop into a chronic active inflammatory lesion.1,2 These unstable plaques are characterized by increased numbers of activated immune/inflammatory cells and increased expression and release of numerous inflammatory mediators and proteolytic enzymes. Thinning of the fibrous cap reflecting reductions in VSMCs and matrix proteins is a key feature of unstable plaques.1,2 The subsequent rupture of weakened unstable plaques, which exposes prothrombotic material from the core of the plaque, is the principal mechanism underlying acute coronary syndromes (ACS) including unstable angina, myocardial infarction, and sudden cardiac death.1,2
Activated macrophages have been considered a primary culprit in destabilizing atherosclerotic plaques. They are a major source of matrix metalloproteinases (MMPs), which can degrade all components of the extracellular matrix and represent a principal mechanism for collagen breakdown and cap weakness.1,2 Macrophages are also highly effective at inducing apoptosis of VSMCs, a characteristic feature of unstable plaques.3,4 Although CD4+ T cells are prominent within unstable plaques, they have generally been
Related Article:
Circ. Res. 2006 98: 1168-1176.