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Updated: Jul 23, 2026

Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus
Published on: December 7, 2013
Macrophages and ceroid in human atherosclerosis
M J Mitchinson1, R Y Ball, K L Carpenter
1Cambridge University Department of Pathology, England.
Insights
Atherosclerosis may be a chronic inflammatory disease driven by harmful macrophages, while smooth muscle cells attempt repair. Macrophage activity might promote plaque oxidation, suggesting potential antioxidant interventions.
Area of Science:
- Cardiovascular Science
- Inflammation Biology
- Cellular Pathology
Background:
- Atherosclerosis is a complex cardiovascular disease.
- The roles of different cell types, like macrophages and smooth muscle cells, are debated.
- Understanding cellular contributions is key to developing effective treatments.
Purpose of the Study:
- To propose atherosclerosis as a chronic inflammatory disease.
- To investigate the detrimental roles of monocyte-derived macrophages.
- To explore the reparative functions of smooth muscle cells.
Main Methods:
- Tabulation of macrophage activities contributing to atherosclerosis.
- Description of observations and experiments.
- Analysis of macrophage-lipoprotein interactions.
Main Results:
- Macrophages may contribute to lipoprotein oxidation within atherosclerotic plaques.
- Significant variation exists in individual macrophage oxidative capacity.
- Smooth muscle cells appear to have a primarily reparative role.
Conclusions:
- Macrophages play a potentially harmful role in atherosclerosis pathogenesis.
- Individual differences in macrophage function could influence disease progression.
- Antioxidant therapies may offer a viable intervention strategy for atherosclerosis.
Abstract:
It is proposed that atherosclerosis is a chronic inflammatory disease in which monocyte-derived macrophages are doing harm and smooth muscle cells are essentially reparative. Activities of macrophages that might be contributory to the development of atherosclerosis are tabulated. Observations and experiments are described that suggest macrophages may be contributing to lipoprotein oxidation within the plaque and that individual humans vary in their macrophage oxidative capacity. The possibility of intervention with antioxidants is discussed.
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