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Exercise Improves Mitochondrial Homeostasis: A Potential Neuroprotective Strategy for Ischemic Stroke
Wenyan Bo1, Qingxiang Guo1, Wanyu Zhu1
1Institute of Physical Education, Shanxi University, Taiyuan 030006, China.
Antioxidants (Basel, Switzerland)
|May 27, 2026
Summary
Regular exercise helps prevent ischemic stroke by maintaining mitochondrial homeostasis. This review details how exercise impacts mitochondrial function to offer new therapeutic strategies for stroke.
Area of Science:
- Exercise physiology
- Neuroscience
- Mitochondrial biology
Background:
- Ischemic stroke pathophysiology involves mitochondrial homeostasis disruption.
- Exercise is known to reduce stroke risk, but mechanisms are unclear.
Purpose of the Study:
- To review exercise's protective effects against ischemic stroke.
- To elucidate the molecular mechanisms linking exercise, mitochondrial homeostasis, and stroke.
Main Methods:
- Systematic review of existing literature.
- Analysis of molecular mechanisms of exercise on mitochondria in stroke.
Main Results:
- Exercise training maintains mitochondrial homeostasis in ischemic stroke.
- Key mechanisms include improved biogenesis, dynamics, redox balance, mitophagy, and transport.
- Exercise attenuates stroke onset and progression.
Conclusions:
- Mitochondrial homeostasis is critical in ischemic stroke pathology.
- Exercise offers promising therapeutic potential for stroke via mitochondrial regulation.
- Further research into exercise-based strategies is warranted.
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