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Related Experiment Video

Updated: Apr 30, 2026

Flow Cytometry Analysis of Immune Cells Within Murine Aortas
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CXCR4 blockade induces atherosclerosis by affecting neutrophil function.

Ilze Bot1, Isabelle T M N Daissormont2, Alma Zernecke3

  • 1Division of Biopharmaceutics, Leiden Academic Centre for Drug Research, Leiden University, Leiden, The Netherlands.

Journal of Molecular and Cellular Cardiology
|May 13, 2014
PubMed
Summary

The SDF-1α/CXCR4 pathway impacts advanced atherosclerosis by affecting neutrophil function. Blocking CXCR4 exacerbates plaque progression and intraplaque hemorrhage, highlighting its role in disease development.

Keywords:
CXCR4SDF-1αatherosclerosisneutrophilssenescence

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Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Atherosclerosis Research

Background:

  • The SDF-1α/CXCR4 signaling pathway is implicated in intimal hyperplasia and early atherosclerosis.
  • Its role in advanced, clinically relevant stages of atherosclerosis requires further investigation.

Purpose of the Study:

  • To investigate the impact of the SDF-1α/CXCR4 dyad on advanced atherosclerosis in mouse models and human patients.
  • To elucidate the specific mechanisms by which CXCR4 influences plaque progression and associated complications.

Main Methods:

  • Immunohistochemical analysis of CXCR4 expression in human atherosclerotic lesions.
  • Reconstitution of LDLr(-/-) mice with bone marrow expressing SDF-1α antagonist or CXCR4 degrakine.
  • Assessment of plaque progression, intraplaque hemorrhage, and neutrophil function following CXCR4 blockade.

Main Results:

  • Progressive accumulation of CXCR4(+) cells observed in human atherosclerotic plaques.
  • CXCR4 blockade in mice led to increased plaque expansion, intraplaque hemorrhage, and augmented endothelial adhesion of neutrophils.
  • Inhibition of CXCR4 function enhanced neutrophil adhesion, reduced apoptosis, and caused hyperactivation of circulating neutrophils.

Conclusions:

  • CXCR4 plays a significant role in the later stages of atherosclerotic plaque progression.
  • Perturbation of neutrophil function by CXCR4 contributes to advanced atherosclerosis and cardiovascular events.