Long-term exercise stabilizes atherosclerotic plaque in ApoE knockout mice

Area of Science:

• Cardiovascular Research
• Exercise Physiology
• Atherosclerosis Research

Background:

• Cardiovascular disease remains a leading cause of mortality globally.
• Exercise is a known preventive therapy, but its precise mechanisms, particularly regarding atherosclerosis, require elucidation.
• Atherosclerotic plaque stabilization is a critical therapeutic goal to prevent cardiovascular events.

Purpose of the Study:

• To investigate the plaque-stabilizing effects of long-term exercise in a mouse model of experimental atherosclerosis.
• To examine the role of the Akt-mediated endothelial nitric oxide synthase (eNOS) phosphorylation pathway in exercise-induced plaque stabilization.

Main Methods:

• Apolipoprotein E-deficient (ApoE(-/-)) mice were subjected to 6 months of swimming exercise or maintained as sedentary controls.
• Atherosclerotic plaque stability was assessed in the aortic sinus using immunohistochemistry.
• Protein levels of Akt, phosphorylated Akt (p-Akt), eNOS, and phosphorylated eNOS (p-eNOS) were quantified via Western blotting.

Main Results:

• Mice that underwent long-term exercise exhibited a more stable atherosclerotic plaque phenotype.
• Exercise led to a decreased macrophage content and an increased smooth muscle cell content within plaques.
• No significant modulation in the protein expression of Akt, p-Akt, eNOS, or p-eNOS was observed in exercised mice.

Conclusions:

• Long-term exercise effectively promotes atherosclerotic plaque stability in ApoE(-/-) mice.
• The Akt-mediated eNOS phosphorylation pathway does not appear to be the primary molecular mechanism underlying exercise-induced plaque stabilization in this model.