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The role of complement activation in atherogenesis: the first 40 years

Sonia I Vlaicu1,2, Alexandru Tatomir1, Violeta Rus3

  • 1Department of Neurology, School of Medicine Baltimore, University of Maryland, 655 W. Baltimore Street, Baltimore, MD, 21201, USA.

Immunologic Research
|June 21, 2015
PubMed

Insights

The complement system, part of innate immunity, drives atherosclerosis by activating terminal complement C5b-9. This complex promotes vascular cell proliferation and lesion formation, accelerating disease progression.

Area of Science:

  • Immunology
  • Cardiovascular Biology
  • Pathogenesis of Atherosclerosis

Background:

  • Atherosclerosis involves lipid accumulation, immune cells, and inflammation.
  • The complement system, a key innate immunity component, plays a role in atherosclerosis induction and progression.

Purpose of the Study:

  • To elucidate the role of complement system activation in atherosclerotic inflammation.
  • To investigate the specific contributions of proximal and terminal complement pathways to atherogenesis.

Main Methods:

  • Review of experimental work on complement system activation in atherosclerotic plaque formation.
  • Analysis of the effects of modified LDL and C-reactive protein on complement activation.
  • Examination of the role of the terminal complement C5b-9 complex and Response gene to complement (RGC)-32 in vascular cell responses.

Main Results:

  • Modified LDL accumulation triggers complement activation, forming the terminal complement C5b-9 complex in atherosclerotic lesions.
  • Sublytic C5b-9 assembly activates and proliferates smooth muscle and endothelial cells, releasing pro-inflammatory cytokines.
  • Response gene to complement (RGC)-32, downstream of C5b-9, drives vascular smooth muscle cell and endothelial proliferation, contributing to lesion formation.
  • The classical complement pathway appears protective, while the terminal complement pathway accelerates atherogenesis.

Conclusions:

  • Complement system activation is integral to atherosclerotic inflammation and plaque development.
  • Terminal complement pathway activation significantly contributes to accelerated atherogenesis.
  • Targeting specific complement pathways may offer therapeutic strategies for atherosclerosis.

Keywords:
AtherosclerosisC5b-9 complement complexComplement activationEndothelial cellsRGC-32Smooth muscle cells

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