Nature versus Number: Monocytes in Cardiovascular Disease
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Updated: Oct 20, 2025

Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
Published on: October 17, 2017
Helen Williams1,2, Corinne D Mack1,2, Stephen C H Li3,4
1Vascular Biology Research Centre, Department of Surgery, Westmead Hospital, Westmead, Sydney, NSW 2145, Australia.
Insights
Monocytes are key to cardiovascular disease (CVD) development. This review examines how monocyte subsets change in CVD and dyslipidemia, and how lipid-lowering treatments affect them, impacting plaque formation.
Area of Science:
- Immunology
- Cardiovascular Medicine
- Atherosclerosis Research
Background:
- Monocyte influx into the vessel wall is crucial for atherosclerotic plaque development in cardiovascular disease (CVD).
- Monocytes exhibit heterogeneity, with distinct classical, intermediate, and nonclassical subsets.
- Elevated proportions of intermediate and nonclassical monocytes are observed in CVD patients, suggesting functional roles beyond mere increased numbers.
Purpose of the Study:
- To explore the nature and number of monocyte subsets in the context of cardiovascular disease (CVD).
- To investigate the emergence of altered monocyte subset proportions and functions in dyslipidemia.
- To assess the impact of lipid-lowering medication on these monocyte alterations and their implications for plaque development.
Main Methods:
- Review of existing literature on monocyte subset dynamics in cardiovascular disease (CVD).
- Analysis of emerging evidence regarding monocyte changes in dyslipidemia.
- Evaluation of the effects of lipid-lowering treatments on monocyte subsets and inflammatory markers.
Main Results:
- Increased percentages of intermediate and nonclassical monocytes are associated with cardiovascular disease (CVD).
- Changes in monocyte proportion and function are linked to dyslipidemia.
- Lipid-lowering medications show potential in reversing some of these observed monocyte alterations.
Conclusions:
- Understanding the specific roles and changes in monocyte subsets is vital for comprehending cardiovascular disease (CVD) pathogenesis.
- Dyslipidemia significantly influences monocyte subset distribution and function, offering therapeutic targets.
- Lipid-lowering therapies may modulate monocyte populations, potentially influencing atherosclerotic plaque development and clinical outcomes.
Abstract:
Monocytes play a key role in cardiovascular disease (CVD) as their influx into the vessel wall is necessary for the development of an atherosclerotic plaque. Monocytes are, however, heterogeneous differentiating from classical monocytes through the intermediate subset to the nonclassical subset. While it is recognized that the percentage of intermediate and nonclassical monocytes are higher in individuals with CVD, accompanying changes in inflammatory markers suggest a functional impact on disease development that goes beyond the increased proportion of these 'inflammatory' monocyte subsets. Furthermore, emerging evidence indicates that changes in monocyte proportion and function arise in dyslipidemia, with lipid lowering medication having some effect on reversing these changes. This review explores the nature and number of monocyte subsets in CVD addressing what they are, when they arise, the effect of lipid lowering treatment, and the possible implications for plaque development. Understanding these associations will deepen our understanding of the clinical significance of monocytes in CVD.
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