Atherosclerotic plaques develop as a consequence of the accumulation of circulating lipid and the subsequent migration of inflammatory cells (macrophages and T-lymphocytes) and VSMCs (vascular smooth muscle cells). Advanced plaques consist of a lipid-rich core, separated from the lumen by a fibrous cap composed of VSMCs, collagen and extracellular matrix. Plaque enlargement ultimately narrows the lumen (stenosis) causing angina. However, recent studies have emphasized that acute coronary syndromes (unstable angina/myocardial infarction) are caused by lesion erosion/rupture with superimposed thrombus formation on often small non-stenotic plaques. Thus current therapies work predominantly on stabilization of plaques rather than plaque regression. Apoptosis (programmed cell death) is increasingly observed as plaques develop, although the exact mechanisms and consequences of apoptosis in the development and progression of atherosclerosis are still controversial. Increased endothelial cell apoptosis may initiate atherosclerosis, whereas apoptosis of VSMCs and macrophages localizes in ‘vulnerable’ lesions, i.e. those most likely to rupture, and at sites of rupture. This review will focus on the regulation of apoptosis of cells within the vasculature, concentrating on the relevance of apoptosis to plaque progression and clinical consequences of vascular cell apoptosis.
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October 2004
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Review Article|
September 24 2004
Role of apoptosis in atherosclerosis and its therapeutic implications
Victoria E. A. STONEMAN;
1Unit of Cardiovascular Medicine, Addenbrooke's Centre for Clinical Investigation, Level 6, Box 110, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, U.K.
Correspondence: Dr Victoria Stoneman (email [email protected]).
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Martin R. BENNETT
Martin R. BENNETT
1Unit of Cardiovascular Medicine, Addenbrooke's Centre for Clinical Investigation, Level 6, Box 110, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, U.K.
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Publisher: Portland Press Ltd
Received:
March 17 2004
Revision Received:
June 07 2004
Accepted:
July 01 2004
Accepted Manuscript online:
July 01 2004
Online ISSN: 1470-8736
Print ISSN: 0143-5221
The Biochemical Society
2004
Clin Sci (Lond) (2004) 107 (4): 343–354.
Article history
Received:
March 17 2004
Revision Received:
June 07 2004
Accepted:
July 01 2004
Accepted Manuscript online:
July 01 2004
Citation
Victoria E. A. STONEMAN, Martin R. BENNETT; Role of apoptosis in atherosclerosis and its therapeutic implications. Clin Sci (Lond) 1 October 2004; 107 (4): 343–354. doi: https://doi.org/10.1042/CS20040086
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