CCR2⁺ macrophages are required for exercise-induced cardiac remodeling

Area of Science:

• Cardiovascular physiology and immunology
• Cardiac remodeling and adaptation
• Macrophage biology in exercise

Background:

• Cardiovascular diseases (CVDs) are a leading cause of death globally.
• Exercise is a promising non-pharmacological intervention for CVDs.
• The role of cardiac macrophages in exercise-induced cardiac remodeling is poorly understood.

Purpose of the Study:

• To investigate the role of C-C motif chemokine receptor 2 (CCR2+) macrophages in exercise-induced cardiac remodeling.
• To examine sex-specific differences in exercise-induced cardiac remodeling.
• To determine if CCR2+ macrophages are essential for exercise-induced cardiac adaptation.

Main Methods:

• Utilized a voluntary wheel-running mouse model.
• Employed diphtheria toxin to deplete CCR2+ macrophages.
• Assessed cardiac remodeling via echocardiography, morphometrics, and tissue analysis.

Main Results:

• Voluntary exercise induced cardiac hypertrophy and preserved cardiac function in mice.
• Increased CCR2+ macrophages were observed in the hearts of exercising mice.
• Depletion of CCR2+ macrophages abolished exercise-induced cardiac hypertrophy and reduced cardiomyocyte stiffness.

Conclusions:

• CCR2+ macrophages are essential mediators of exercise-induced cardiac remodeling.
• Immune-cardiac interactions involving CCR2+ macrophages are critical for exercise adaptation.
• Findings provide novel insights into the mechanisms of exercise-induced cardiac adaptation.