Cardiovascular disease predictors and adipose tissue macrophage polarization: Is there a link?

Ivana Kralova Lesna1, Marek Petras2, Sona Cejkova1

  • 11 Laboratory for Atherosclerosis Research, Institute for Clinical and Experimental Medicine, Czech Republic.

Insights

Cardiovascular risk factors like age, male sex, and high cholesterol influence pro-inflammatory macrophages in visceral fat. Statin therapy reduces these inflammatory cells, offering a potential therapeutic target for cardiovascular disease.

Area of Science:

  • Immunology
  • Cardiovascular Science
  • Metabolic Disease

Background:

  • Cardiovascular disease (CVD) risk is linked to adipose tissue inflammation.
  • Understanding the role of macrophage subsets in adipose tissue is crucial for CVD pathophysiology.

Purpose of the Study:

  • To analyze the relationship between cardiovascular risk predictors and pro-inflammatory and anti-inflammatory macrophages in human adipose tissue.
  • To investigate the impact of statin therapy on these macrophage subsets.

Main Methods:

  • Subcutaneous and visceral adipose tissues were obtained from 79 subjects.
  • Macrophage subsets were isolated and analyzed by flow cytometry using specific monoclonal antibodies (CD14, CD16, CD36, CD163).
  • Analysis focused on phagocytic pro-inflammatory, anti-inflammatory, and transitional macrophage subsets in relation to CVD risk factors.

Main Results:

  • Age, male sex, and hypercholesterolemia were positively associated with pro-inflammatory macrophages in visceral adipose tissue.
  • Body mass index showed a positive association with pro-inflammatory macrophages in subcutaneous adipose tissue only.
  • Statin therapy significantly decreased the proportion of pro-inflammatory macrophages.

Conclusions:

  • Cardiovascular risk predictors differentially affect adipose tissue macrophage subpopulations.
  • Pro-inflammatory macrophages in visceral fat are linked to age, male sex, and hypercholesterolemia.
  • Statin treatment demonstrates a beneficial effect by reducing pro-inflammatory macrophages, suggesting a therapeutic avenue for CVD.

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