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Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
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Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions

Published on: October 17, 2017

Thematic review series: the immune system and atherogenesis. Molecular mechanisms regulating monocyte recruitment in

Oswald Quehenberger1

  • 1Department of Medicine, University of California, San Diego, La Jolla, CA 92093-0682, USA. oquehenberger@ucsd.edu

Journal of Lipid Research
|June 18, 2005
PubMed

Insights

Cardiovascular disease involves inflammatory cell recruitment to artery walls. Understanding monocyte accumulation in atherosclerotic plaques offers new therapeutic targets for this leading cause of death.

Area of Science:

  • Cardiovascular Science
  • Immunology
  • Pathology

Background:

  • Cardiovascular disease, marked by arterial lipid buildup, is a major cause of mortality.
  • Atherogenesis initiates with inflammatory cell recruitment into developing arterial lesions.
  • Inflammatory mediators play a crucial role in cardiovascular disease initiation and progression.

Purpose of the Study:

  • To review the mechanisms of inflammatory cell recruitment in atherosclerosis.
  • To elucidate the process of monocyte accumulation within atherosclerotic plaques.
  • To highlight potential therapeutic targets based on cellular recruitment pathways.

Main Methods:

  • Review of experimental research on inflammatory cell recruitment.
  • Analysis of adhesion proteins and chemokines involved in monocyte migration.
  • Synthesis of current understanding of monocyte retention in atherosclerotic lesions.

Main Results:

  • Significant progress in understanding monocyte, macrophage, and T-cell accumulation in plaques.
  • Identification of key adhesion proteins and chemokines mediating inflammatory cell recruitment.
  • Development of a mechanistic framework for therapeutic interventions.

Conclusions:

  • Inflammatory cell recruitment is central to atherogenesis.
  • Understanding these mechanisms provides a basis for novel cardiovascular disease therapies.
  • Targeting monocyte recruitment and retention pathways holds therapeutic promise.

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