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Alternative C3 Complement System: Lipids and Atherosclerosis.

Maisa Garcia-Arguinzonis1, Elisa Diaz-Riera1, Esther Peña1,2

  • 1Cardiovascular Program-ICCC, Research Institute-Hospital Santa Creu i Sant Pau, IIB-Sant Pau, 08025 Barcelona, Spain.

International Journal of Molecular Sciences
|June 2, 2021
PubMed
Summary
This summary is machine-generated.

The C3 complement system plays a local role in atherosclerosis progression in Familial Hypercholesterolemia (FH) by influencing vascular smooth muscle cells, independent of circulating levels.

Keywords:
atherosclerosiscardiovascular diseasecomplement systemmass spectrometryproteomics

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Area of Science:

  • Immunology and Cardiovascular Science
  • Systems Biology and Proteomics
  • Complement System and Atherosclerosis

Background:

  • Familial Hypercholesterolemia (FH) is linked to inflammation, persisting despite lipid-lowering therapies.
  • The C3 complement system (C3) is an inflammatory mediator implicated in atherosclerosis (AT), but its role alongside lipids in plaque progression is unclear.
  • Understanding C3's local effects in FH is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the role of C3 in relation to lipoprotein levels during atherosclerosis progression using a systems biology approach.
  • To understand the effects of C3 products on the phenotype and function of human lipid-loaded vascular smooth muscle cells (VSMCs).

Main Methods:

  • Mass spectrometry and differential proteomics to analyze human aortic extracellular matrix (ECM).
  • Computed tomographic angiography to assess coronary atherosclerosis in FH patients.
  • Cell culture studies of human VSMCs, including RT-PCR and Western blot analysis.

Main Results:

  • Human atherosclerotic-ECM is enriched in active C3 complement components, with higher C3 product abundance compared to normal segments.
  • Circulating C3 levels are elevated in FH patients with subclinical coronary AT, but not correlated with plaque burden, suggesting local regulation.
  • Lipid-loaded VSMCs upregulate C3, and active C3 fragments (C3a, iC3b) modulate VSMC migration, spreading, and adhesion.

Conclusions:

  • The C3 complement system is locally regulated within the arterial wall in atherosclerosis.
  • Active C3 fragments influence VSMC behavior, impacting vascular remodeling and atherosclerotic plaque progression in FH.
  • This study highlights the C3 complement system's significant role in the pathophysiology of advanced human atherosclerotic lesions.