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Updated: May 25, 2026

Depletion and Reconstitution of Macrophages in Mice
Published on: August 1, 2012
Therapeutic strategies to deplete macrophages in atherosclerotic plaques
Inge De Meyer1, Wim Martinet, Guido R Y De Meyer
1Division of Physiopharmacology, University of Antwerp, Antwerp, Belgium. guido.demeyer@ua.ac.be
Insights
Macrophages are key in atherosclerosis development and plaque instability. Strategies to deplete these cells, by reducing inflammation or inducing cell death, may stabilize plaques.
Area of Science:
- Cardiovascular Research
- Immunology
- Pathology
Background:
- Macrophages play a central role throughout all stages of atherosclerosis.
- Monocyte recruitment continuously fuels this chronic inflammatory cardiovascular disease.
- Macrophage accumulation contributes significantly to atherosclerotic plaque development, progression, and destabilization.
Purpose of the Study:
- To review strategies for depleting macrophages from atherosclerotic plaques.
- To discuss interventions aimed at promoting atherosclerotic plaque stabilization by targeting macrophages.
Main Methods:
- Review of current therapeutic strategies targeting macrophage involvement in atherosclerosis.
- Analysis of methods to reduce inflammatory stimuli, modulate adhesion molecules, and induce macrophage death within plaques.
Main Results:
- Several intervention strategies exist to modulate macrophage populations in atherosclerosis.
- Targeting lipid metabolism, adhesion molecules, chemokines, and inducing macrophage apoptosis are discussed.
Conclusions:
- Depleting macrophages from atherosclerotic plaques is a promising therapeutic approach.
- Combined strategies involving anti-inflammatory drugs and macrophage-targeted therapies may enhance plaque stabilization.
Abstract:
Macrophages can be found in all stages of atherosclerosis and are major contributors of atherosclerotic plaque development, progression and destabilization. Continuous recruitment of monocytes drives this chronic inflammatory disease, which can be intervened by several strategies: reducing the inflammatory stimulus by lowering circulating lipids and promoting cholesterol efflux from plaque, direct and indirect targeting of adhesion molecules and chemokines involved in monocyte adhesion and transmigration and inducing macrophage death in atherosclerotic plaques in combination with anti-inflammatory drugs. This review discusses the outlined strategies to deplete macrophages from atherosclerotic plaques to promote plaque stabilization.
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