The Effect of Granulocyte Colony-Stimulating Factor on the Progression of Atherosclerosis in Animal Models: A

Manli Liu1,2, Kejian Liu3,4, Dongdong Chen1,2

  • 1Department of Pathology and Key Laboratory of Xinjiang Endemic and Ethnic Diseases, Ministry of Education, Shihezi University School of Medicine, Shihezi, Xinjiang, China.

Insights

Granulocyte colony-stimulating factor (G-CSF) therapy may reduce atherosclerosis progression by decreasing lesion area in animal models. This finding offers insights for future preclinical and clinical studies on G-CSF for atherosclerosis treatment.

Area of Science:

  • Cardiovascular Research
  • Regenerative Medicine
  • Inflammatory Diseases

Background:

  • Atherosclerosis is a prevalent inflammatory condition affecting arteries.
  • Stem cell therapies show promise in improving cardiac function post-myocardial infarction.
  • Granulocyte colony-stimulating factor (G-CSF) mobilizes stem cells, suggesting potential therapeutic applications for atherosclerosis.

Purpose of the Study:

  • To evaluate the efficacy of G-CSF in inhibiting atherosclerosis progression using a meta-analysis of animal models.
  • To provide a reference for preclinical research and future human clinical trials investigating G-CSF for atherosclerosis.

Main Methods:

  • A systematic literature search was conducted across multiple databases.
  • A meta-analysis of seven relevant studies was performed using a random-effect model.
  • Statistical analyses were executed using Review Manager Version 5.2 and Stata 12.0.

Main Results:

  • G-CSF therapy demonstrated a significant reduction in atherosclerotic lesion area (WMD: 7.29%, P=0.006).
  • No significant impact of G-CSF on serum cholesterol or triglyceride levels was observed (P>0.54).
  • Animal type (e.g., rabbits) and G-CSF administration frequency (>20) were identified as significant factors influencing lesion area changes via metaregression analysis.

Conclusions:

  • G-CSF treatment shows potential in inhibiting the progression of atherosclerosis in preclinical animal models.
  • Further research is warranted to translate these findings into effective human therapies for atherosclerosis.
Abstract

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