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Macrophage death and the role of apoptosis in human atherosclerosis

L Hegyi1, S J Hardwick, R C Siow

  • 1Division of Cardiovascular Medicine, Department of Medicine, ACCI, Addenbrooke's Hospital, Cambridge, CB2 2QQ, UK. lhegyi@mole.bio.cam.ac.uk

Journal of Hematotherapy & Stem Cell Research
|March 29, 2001
PubMed

Insights

Atherosclerosis is an inflammatory arterial disease. Macrophage death, particularly apoptosis, and oxidized LDL contribute to its development, suggesting potential therapeutic strategies like gene therapy.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Pathogenesis of Atherosclerosis

Background:

  • Atherosclerosis is a leading cause of death in Western populations, characterized by arterial inflammation.
  • Key cellular players include smooth muscle cells, macrophages, and T lymphocytes.
  • The complete pathogenesis remains under investigation, but inflammation and specific risk factors are implicated.

Purpose of the Study:

  • To review the function of macrophages in atherosclerosis.
  • To discuss the significance of macrophage death, including apoptosis, in the disease process.
  • To explore therapeutic strategies for preventing atherosclerosis complications.

Main Methods:

  • Review of experimental and clinical studies.
  • Analysis of in vitro evidence regarding oxidized low-density lipoprotein (LDL).
  • Discussion of therapeutic approaches such as bone marrow transplantation and gene therapy.

Main Results:

  • Evidence suggests atherosclerosis is an inflammatory disease involving macrophages.
  • Oxidized LDL is implicated as atherogenic, potentially inducing apoptosis and DNA damage in intimal cells.
  • Macrophage apoptosis plays a significant role in the disease's progression.

Conclusions:

  • Macrophage function and death are critical in atherosclerosis.
  • Oxidized LDL contributes to atheroma formation and cell death.
  • Therapeutic strategies targeting these mechanisms may prevent cardiovascular events like heart attack and stroke.

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