Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:2255-2264
Published online before print September 1, 2005, doi: 10.1161/01.ATV.0000184783.04864.9f
Published online before print September 1, 2005, doi: 10.1161/01.ATV.0000184783.04864.9f
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© 2005 American Heart Association, Inc.
Brief Reviews |
Consequences and Therapeutic Implications of Macrophage Apoptosis in Atherosclerosis
The Importance of Lesion Stage and Phagocytic Efficiency
From the Departments of Medicine, Anatomy & Cell Biology, and Physiology & Cellular Biophysics, Columbia University, New York.
Correspondence to Ira Tabas, Department of Medicine, Columbia University, 630 W 168th St, New York, NY 10032. E-mail iat1{at}columbia.edu
Macrophage apoptosis occurs throughout all stages of atherosclerosis, yet new findings in vivo suggest that the consequences of this event may be very different in early versus late atherosclerotic lesions. In early lesions, where phagocytic clearance of apoptotic cells appears to be efficient, macrophage apoptosis is associated with diminished lesion cellularity and decreased lesion progression. In late lesions, however, a number of factors may contribute to defective phagocytic clearance of apoptotic macrophages, leading to secondary necrosis of these cells and a proinflammatory response. The cumulative effect of these late lesional events is generation of the necrotic core, which, in concert with proatherogenic effects of residual surviving macrophages, promotes further inflammation, plaque instability, and thrombosis. Thus, the ability or lack thereof of lesional phagocytes to safely clear apoptotic macrophages may be an important determinant of acute atherothrombotic clinical events. Further understanding of the mechanisms involved in macrophage apoptosis and phagocytic clearance might lead to novel therapeutic strategies directed against the progression of advanced plaques.
Whereas macrophage apoptosis in early atherosclerotic lesions appears to decrease lesion cellularity, macrophage apoptosis in advanced lesions may contribute to necrotic core formation. This difference is probably attributable to the relatively incompetence of late lesional phagocytes to safely and efficiently clear apoptotic cells, leading to postapoptotic macrophage necrosis.
Key Words: atherosclerosis • macrophage • apoptosis • phagocytosis • inflammation
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A. Baldan, L. Pei, R. Lee, P. Tarr, R. K. Tangirala, M. M. Weinstein, J. Frank, A. C. Li, P. Tontonoz, and P. A. Edwards Impaired Development of Atherosclerosis in Hyperlipidemic Ldlr-/- and ApoE-/- Mice Transplanted With Abcg1-/- Bone Marrow Arterioscler Thromb Vasc Biol, October 1, 2006; 26(10): 2301 - 2307. [Abstract] [Full Text] [PDF]
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A. Tuominen, Y. I. Miller, L. F. Hansen, Y. A. Kesaniemi, J. L. Witztum, and S. Horkko A Natural Antibody to Oxidized Cardiolipin Binds to Oxidized Low-Density Lipoprotein, Apoptotic Cells, and Atherosclerotic Lesions Arterioscler Thromb Vasc Biol, September 1, 2006; 26(9): 2096 - 2102. [Abstract] [Full Text] [PDF]
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V. A. Korshunov, A. M. Mohan, M. A. Georger, and B. C. Berk Axl, A Receptor Tyrosine Kinase, Mediates Flow-Induced Vascular Remodeling Circ. Res., June 9, 2006; 98(11): 1446 - 1452. [Abstract] [Full Text] [PDF]
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 M. Twickler, G. Dallinga-Thie, and M.-J. Cramer Trojan horse hypothesis: inhaled airborne particles, lipid bullets, and atherogenesis. JAMA, May 24, 2006; 295(20): 2354 - 2354. [Full Text] [PDF]
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A. Boullier, Y. Li, O. Quehenberger, W. Palinski, I. Tabas, J. L. Witztum, and Y. I. Miller Minimally Oxidized LDL Offsets the Apoptotic Effects of Extensively Oxidized LDL and Free Cholesterol in Macrophages Arterioscler Thromb Vasc Biol, May 1, 2006; 26(5): 1169 - 1176. [Abstract] [Full Text] [PDF]
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Y. Li, M.-C. Gerbod-Giannone, H. Seitz, D. Cui, E. Thorp, A. R. Tall, G. K. Matsushima, and I. Tabas Cholesterol-induced Apoptotic Macrophages Elicit an Inflammatory Response in Phagocytes, Which Is Partially Attenuated by the Mer Receptor J. Biol. Chem., March 10, 2006; 281(10): 6707 - 6717. [Abstract] [Full Text] [PDF]
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