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Atherosclerosis: role of chemokines and macrophages

A D Lucas1, D R Greaves

  • 1Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford, OX1 3RE, UK. andrew.lucas@path.ox.ac.uk

Expert Reviews in Molecular Medicine
|October 31, 2003
PubMed

Insights

This review explores atherosclerosis, a major artery disease causing heart attacks and stroke. It highlights macrophage biology and chemokines

Area of Science:

  • Cardiovascular pathology
  • Immunology
  • Cell biology

Background:

  • Atherosclerosis is a major arterial disease underlying heart attacks, stroke, and peripheral artery disease.
  • Early lesions (fatty streaks) involve macrophage foam cells from monocytes.
  • Advanced lesions (fibro-fatty plaques) result from monocyte recruitment and smooth muscle cell proliferation.

Purpose of the Study:

  • To review key features of macrophage biology in atherosclerosis.
  • To discuss factors influencing atherosclerotic lesion development (atherogenesis).
  • To explore the role of chemokines in monocyte recruitment and macrophage differentiation.

Main Methods:

  • Literature review of atherosclerosis pathogenesis.
  • Analysis of macrophage biology and function.
  • Examination of chemokine involvement in monocyte recruitment.

Main Results:

  • Macrophage foam cells are central to early atherosclerotic lesions.
  • Smooth muscle cell migration and proliferation contribute to advanced plaques.
  • T helper cell cytokines modulate macrophage gene expression.

Conclusions:

  • Understanding macrophage biology is crucial for addressing atherosclerosis.
  • Chemokines play a significant role in mediating monocyte recruitment and macrophage differentiation.
  • Further research into chemokines may offer therapeutic targets for atherosclerosis.

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