Exercise as a therapeutic strategy against mitochondrial dysfunction in ischemic stroke: Molecular mechanisms and...

Ischemic stroke (IS) is a leading cause of disability and mortality worldwide, with mitochondrial dysfunction being a fundamental pathological mechanism. This dysfunction involves a dynamic imbalance, diminished biosynthesis, oxidative stress, and dysregulated autophagy. Exercise, a promising non-pharmacological intervention, can ameliorate this dysfunction, but its precise molecular mechanisms remain to be fully elucidated. This review synthesizes evidence demonstrating that exercise enhances mitochondrial morphology and function through various pathways, including the promotion of mitochondrial biogenesis, the regulation of mitochondrial ROS, and the modulation of mitochondrial dynamics and mitophagy, thereby mitigating functional impairments associated with IS. Critically, the beneficial effects of exercise are dose dependent, highlighting the necessity for personalized exercise prescriptions on the basis of individual patient profiles. Elucidating these mechanisms provides a crucial theoretical foundation for developing exercise-based strategies for the prevention and treatment of IS.