Nature versus Number: Monocytes in Cardiovascular Disease

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.

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