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Published on: May 24, 2019

Mechanisms and consequences of macrophage apoptosis in atherosclerosis

Tracie Seimon1, Ira Tabas

  • 1Department of Medicine, Columbia University, New York, NY 10032, USA.

Journal of Lipid Research
|October 28, 2008
PubMed

Insights

Macrophage apoptosis plays dual roles in atherosclerosis, limiting early lesions but promoting advanced plaque complications. Efferocytosis and ER stress/PRR pathways influence these outcomes.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Pathology

Background:

  • Macrophage apoptosis is integral to atherosclerotic plaque development.
  • Apoptosis exhibits dichotomous roles, influencing early and advanced lesion progression.
  • Understanding macrophage death mechanisms is crucial for atherosclerosis research.

Purpose of the Study:

  • To review the dual roles of macrophage apoptosis in atherosclerosis.
  • To examine the impact of efferocytosis on apoptotic macrophages in lesions.
  • To explore molecular mechanisms, including ER stress and PRRs, in macrophage apoptosis.

Main Methods:

  • Literature review of research on macrophage apoptosis in atherosclerosis.
  • Analysis of studies on efferocytosis in early and advanced lesions.
  • Examination of molecular pathways (ER stress, PRRs) governing macrophage death.

Main Results:

  • Macrophage apoptosis limits cellularity in early lesions, suppressing progression.
  • In advanced lesions, apoptosis contributes to necrotic core formation, increasing plaque vulnerability.
  • Efferocytosis dynamics and ER stress/PRR signaling are key regulators.

Conclusions:

  • Macrophage apoptosis has context-dependent effects on atherosclerosis.
  • Efferocytosis modulates the impact of apoptosis in different lesion stages.
  • ER stress and PRR pathways are critical inducers of macrophage apoptosis in this disease.

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