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Quantification of Monocyte Chemotactic Activity In Vivo and Characterization of Blood Monocyte Derived Macrophages
09:57

Quantification of Monocyte Chemotactic Activity In Vivo and Characterization of Blood Monocyte Derived Macrophages

Published on: August 12, 2019

Molecular and cellular mechanisms of macrophage survival in atherosclerosis

Wim Martinet1, Dorien M Schrijvers, Guido R Y De Meyer

  • 1Laboratory of Physiopharmacology, University of Antwerp, Belgium. wim.martinet@ua.ac.be

Basic Research in Cardiology
|September 13, 2012
PubMed

Insights

Macrophages in atherosclerosis survive and proliferate via antioxidant protection, anti-apoptotic proteins, and cellular mechanisms like autophagy. These survival strategies contribute to plaque growth and destabilization.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Cellular Pathology

Background:

  • Macrophages are central to atherosclerotic plaque development and progression.
  • Despite cell death from atherogenic stressors, advanced plaques exhibit high macrophage content.
  • Macrophage accumulation results from monocyte recruitment, reduced emigration, and impaired efferocytosis.

Purpose of the Study:

  • To review macrophage survival mechanisms within advanced atherosclerotic plaques.
  • To elucidate how these mechanisms contribute to plaque growth and destabilization.

Main Methods:

  • Literature review of cellular and molecular mechanisms.
  • Analysis of macrophage responses to atherogenic stressors.
  • Examination of survival pathways including antioxidant defenses, anti-apoptotic signaling, unfolded protein response, and autophagy.

Main Results:

  • Macrophages employ enhanced antioxidant protection via organic molecules and enzymes.
  • Upregulation of anti-apoptotic protein synthesis supports macrophage survival.
  • Activation of cellular protection mechanisms like unfolded protein response and autophagy promotes macrophage persistence.

Conclusions:

  • Macrophage survival strategies are critical for the growth of advanced atherosclerotic plaques.
  • These survival mechanisms contribute to plaque destabilization and progression.
  • Understanding these pathways is key to developing novel therapeutic interventions for atherosclerosis.

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