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Updated: Dec 12, 2025

Quantification of Atherosclerosis in Mice
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Quantification of Atherosclerosis in Mice

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Protective Role of C3aR (C3a Anaphylatoxin Receptor) Against Atherosclerosis in Atherosclerosis-Prone Mice

Lin-Lin Wei1, Ning Ma1, Kun-Yi Wu1

  • 1From the Core Research Laboratory (L.-L.W., N.M., K.-Y.W., J.-X.W., T.-Y.D., S.-J.Z., K.L.), Xi'an Jiaotong University, China.

Arteriosclerosis, Thrombosis, and Vascular Biology
|August 9, 2020
PubMed
Abstract

Insights

The C3a anaphylatoxin receptor (C3aR) plays a protective role in atherosclerosis. Its absence exacerbates disease by increasing inflammation and promoting pro-inflammatory M1 macrophage polarization.

Area of Science:

  • Immunology
  • Cardiovascular Biology
  • Complement System

Background:

  • Emerging evidence indicates protective roles for C3a anaphylatoxin receptor (C3aR) signaling in inflammatory diseases.
  • The specific role of C3aR in atherosclerosis remains largely unknown.

Purpose of the Study:

  • To investigate the potential protective role of C3aR in aortic atherosclerosis.
  • To explore the underlying molecular and cellular mechanisms involved in C3aR-mediated protection.

Main Methods:

  • Generation of C3aR-deficient/ApoE-deficient (C3ar-/-/Apoe-/-) mice by cross-breeding.
  • Assessment of atherosclerotic plaque burden, aortic tissue inflammation, leukocyte infiltration, and systemic inflammatory responses in mice fed a high-fat diet for 16 weeks.
  • In vitro analysis of peritoneal macrophages stimulated with C3a.

Main Results:

  • C3ar-/-/Apoe-/- mice exhibited more severe atherosclerosis compared to Apoe-/- controls.
  • Absence of C3aR led to increased local production of pro-inflammatory mediators (CCL2, TNF-α) and enhanced monocyte/macrophage infiltration with an M1-like phenotype in aortic lesions.
  • Mice lacking C3aR showed heightened systemic inflammatory responses, including elevated plasma CCL2 and TNF-α levels.
  • In vitro, C3a stimulation promoted anti-inflammatory M2 macrophage polarization while suppressing M1 polarization.

Conclusions:

  • C3aR plays a protective role in the development of atherosclerosis.
  • The C3a/C3aR axis confers protection by negatively regulating pro-inflammatory responses.
  • C3aR modulates macrophage polarization towards an anti-inflammatory phenotype, thereby mitigating atherosclerosis.
Keywords:
atherosclerosiscomplement C3a receptorinflammationmacrophages

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