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[Thrombosis and apoptosis]

H Takeya1, Y Tanaka, K Suzuki

  • 1Department of Molecular Pathobiology, Mie University School of Medicine, Tsu.

Rinsho Byori. the Japanese Journal of Clinical Pathology
|July 1, 1997
PubMed
Summary
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Apoptosis, a form of programmed cell death, promotes blood clot formation and atherosclerotic plaque instability. Understanding these links is crucial for managing thrombophilia and cardiovascular disease.

Area of Science:

  • Cell Biology
  • Pathophysiology
  • Immunology

Context:

  • Apoptosis is a fundamental biological process involved in tissue homeostasis and disease.
  • Thrombophilia, characterized by an increased tendency to form blood clots, is linked to various pathological conditions.
  • Atherosclerosis involves plaque buildup in arteries, increasing the risk of heart attack and stroke.

Purpose:

  • This review elucidates the intricate mechanisms connecting apoptosis to the activation of blood coagulation and atherosclerotic plaque instability.
  • It explores how apoptotic cells contribute to thrombus formation and the development of thrombotic disorders.
  • The review also examines the bidirectional relationship between anti-phospholipid antibodies and apoptosis.

Summary:

  • Apoptotic cells exhibit procoagulant activity, particularly on surface blebs, promoting thrombus formation.

Related Experiment Videos

  • Anti-phospholipid antibodies can induce apoptosis, leading to immunogenic and procoagulant blebs.
  • Apoptosis of inflammatory cells within atherosclerotic plaques contributes to plaque instability and rupture.
  • Endothelial cell apoptosis results in loss of anticoagulant properties and increased leukocyte adhesion, accelerating atherosclerosis.

    • Impact:

    • This review provides a comprehensive understanding of apoptosis's role in thrombophilia and atherosclerosis.
    • It highlights potential therapeutic targets for managing thrombotic disorders and cardiovascular diseases.
    • The findings underscore the importance of considering apoptosis in the context of thrombosis and plaque progression.