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The complement system in atherosclerosis.

P S Seifert1, M D Kazatchkine

  • 1Department of Clinical Chemistry, Sahlgren's Hospital, Gothenburg, Sweden.

Atherosclerosis
|October 1, 1988
PubMed
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The complement system, a part of immunity, is activated in atherosclerosis and myocardial infarction. Its activation products influence lesion development and heart attack severity.

Area of Science:

  • Immunology
  • Cardiovascular Biology
  • Pathology

Background:

  • The complement system is a crucial part of innate immunity, involving plasma proteins, receptors, and regulatory molecules.
  • Complement activation culminates in the formation of C5b-9 terminal complexes, implicated in various pathological conditions.
  • These complexes have been detected in human atherosclerotic lesions, suggesting a role in the disease.

Purpose of the Study:

  • To investigate the role of complement activation in the pathogenesis of atherosclerosis and its complications.
  • To explore the effects of complement activation products on lesion development and myocardial infarction outcomes.
  • To understand the regulation of complement activation within atherosclerotic lesions.

Main Methods:

  • Immunohistochemistry to detect complement complexes (C5b-9) and proteins (C3, C4) in human atherosclerotic lesions and cardiac myocytes.

Related Experiment Videos

  • In vitro studies using cholesterol and oxysterols to assess their complement-activating properties.
  • Experimental models of myocardial ischemia to evaluate the effects of decomplementation on infarct size and inflammation.

    • Main Results:

    • Endothelial cells in atherosclerotic lesions and cardiac myocytes post-myocardial infarction show complement protein deposition (C3, C4, C5b-9).
    • Cholesterol and oxysterols can activate the complement system in vitro.
    • Experimental reduction of complement (decomplementation) decreased infarct size and inflammatory cell infiltration in a model of myocardial ischemia.

    Conclusions:

    • The complement system is activated in atherosclerosis and myocardial infarction, playing a role in disease pathogenesis and progression.
    • Complement activation products may influence macrophage function and lesion development, though mechanisms require further elucidation.
    • Further research is needed to fully understand the complex role and regulation of complement in cardiovascular diseases.