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Updated: May 18, 2026
07:05
Mouse Model of Alloimmune-induced Vascular Rejection and Transplant Arteriosclerosis
Published on: May 17, 2015
Macrophage proliferation and apoptosis in atherosclerosis
Vicente Andrés1, Oscar M Pello, Carlos Silvestre-Roig
1Department of Epidemiology, Atherothrombosis and Imaging, Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.
Current Opinion in Lipidology
|September 12, 2012
Summary
Macrophage proliferation and apoptosis regulate immune cell accumulation in atherosclerosis. Understanding these processes in atherosclerotic plaques is key for developing new treatments for atherothrombosis.
Area of Science:
- Cardiovascular Research
- Immunology
- Cell Biology
Background:
- Atherosclerosis involves immune cell infiltration and differentiation into macrophages within blood vessel walls.
- Macrophage subtypes exhibit protective or pathogenic roles in vascular lesions.
- Cardiovascular risk factors drive these cellular processes.
Purpose of the Study:
- To review current knowledge on molecular mechanisms regulating macrophage proliferation and apoptosis in atherosclerotic plaques.
- To understand how these processes influence macrophage number and function.
Main Methods:
- Review of existing scientific literature on macrophage biology in atherosclerosis.
- Analysis of molecular mechanisms governing proliferation and apoptosis in lesional macrophages.
- Examination of studies involving genetic manipulation in mouse models.
Main Results:
- Lesional macrophages initially limit atherosclerosis by clearing debris.
- In advanced lesions, macrophages promote chronic inflammation, increasing risks of myocardial infarction and stroke.
- Modulating macrophage proliferation and apoptosis impacts plaque burden in experimental models.
Conclusions:
- While progress has been made, the therapeutic benefit of manipulating macrophage proliferation and apoptosis in atherosclerosis remains uncertain.
- Further research may lead to novel therapies for preventing and treating atherothrombosis.
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