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Updated: Jun 21, 2026

Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
Published on: October 17, 2017
The fate of monocytes in atherosclerosis
1Department of Gene and Cell Medicine, and the Immunology Institute, Mount Sinai School of Medicine, New York, NY 10029, USA. gwendalyn.randolph@mssm.edu
Insights
Monocytes are key inflammatory cells in atherosclerosis. Targeting these cells offers potential therapeutic strategies by modulating their phenotype, recruitment, survival, or egress from plaques to resolve inflammation.
Area of Science:
- Immunology
- Cardiovascular Biology
- Pathology
Background:
- Monocytes are the primary inflammatory cells infiltrating atherosclerotic plaques.
- Monocyte recruitment into plaques is a critical driver of atherosclerosis progression.
Purpose of the Study:
- To discuss potential therapeutic intervention points targeting monocytes in atherosclerosis.
- To explore strategies for modulating monocyte phenotype, recruitment, survival, and egress.
Main Methods:
- Review of existing literature on monocyte function in atherosclerosis.
- Discussion of potential therapeutic targets and strategies.
Main Results:
- Monocyte involvement in atherosclerosis is multifaceted, offering several intervention points.
- Targeting monocyte subpopulations, recruitment, survival, and egress are all viable therapeutic avenues.
Conclusions:
- Modulating monocyte behavior presents a promising strategy for treating atherosclerosis.
- Further research into specific interventions targeting monocytes is warranted.
Abstract:
Monocytes are the primary inflammatory cell type that infiltrates early atherosclerotic plaques. Their recruitment into plaques drives disease progression. Disease interventions that target monocytes could act at several points: alteration in the phenotype of circulating monocyte subpopulations; reduced recruitment of monocytes into plaques; alterations in the survival of monocyte-derived cells in atherosclerosis; and promotion of migratory egress from plaques to bring about resolution of the plaque inflammatory response. All of these points of intervention will be briefly discussed in this article.
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