Macrophage-mediated CXCL2 regulation of EPC homing promotes the progression of atherosclerosis

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Optical Coherence Tomography Based Biomechanical Fluid-Structure Interaction Analysis of Coronary Atherosclerosis Progression
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Optical Coherence Tomography Based Biomechanical Fluid-Structure Interaction Analysis of Coronary Atherosclerosis Progression

Published on: January 15, 2022

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Jingting Mai1, Runlu Sun1, Wenhao Liu1

  • 1Sun Yat-Sen University Sun Yat-sen Memorial Hospital, Guangzhou, Guangdong, China.

Cytokine
|January 19, 2026
PubMed

Insights

Macrophages release CXCL2, a key driver of endothelial progenitor cell (EPC) homing in atherosclerosis. Targeting CXCL2 may stabilize atherosclerotic plaques by reducing pathological angiogenesis and plaque progression.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Vascular Biology

Background:

  • Atherosclerosis is a chronic inflammatory disease characterized by pathological angiogenesis and plaque instability.
  • Endothelial progenitor cells (EPCs) play a complex role in atherosclerosis, potentially exacerbating plaque burden and neovascularization.
  • Macrophages are key immune cells involved in atherosclerotic plaque development and inflammation.

Purpose of the Study:

  • To investigate the role of macrophage-derived CXCL2 in mediating endothelial progenitor cell (EPC) homing during atherosclerosis progression.
  • To determine if targeting CXCL2 can modulate EPC recruitment and stabilize atherosclerotic plaques.

Main Methods:

  • Utilized ApoE-/- mice on a high-fat diet and in vitro co-culture models.
  • Employed transcriptome sequencing to identify key mediators of EPC function.
  • Performed in vivo silencing of CXCL2 to assess its functional impact on atherosclerosis.

Main Results:

  • Infused EPCs exacerbated plaque burden, neovascularization, and matrix degradation in a mouse model.
  • Macrophages were essential for EPC recruitment to atherosclerotic plaques.
  • Macrophage-derived CXCL2 was identified as a critical mediator, enhancing EPC angiogenic functions and promoting plaque progression.
  • In vivo silencing of CXCL2 attenuated EPC homing, reduced plaque size and lipid accumulation, decreased neovascularization, and stabilized the plaque matrix.

Conclusions:

  • Macrophage-derived CXCL2 promotes pathological angiogenesis and plaque progression in atherosclerosis by mediating EPC homing.
  • Targeting CXCL2 represents a potential therapeutic strategy for stabilizing atherosclerotic plaques and managing cardiovascular disease.

Keywords:
AtherosclerosisCXCL2Endothelial progenitor cellsMacrophage

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