Research Progress on the Role of Mitochondrial Autophagy in the Prevention and Treatment of Parkinson’s Disease through Exercise
ZHOU Guolong1, RAN Runxin1, ZHOU Wenhui2 *
PD (Parkinson’s disease) is the second most prevalent neurodegenerative disease in the world, and progressive loss of DA (dopamine) ergic neurons and specific accumulation of α-Syn (α-synuclein) in the SNpc (substantia nigra pars compacta) are typical pathological features of PD. Mitophagy dysfunction is a key link driving PD progression. Mitophagy is able to maintain neuronal health and prevent neuronal death by removing and recycling damaged mitochondria and restoring mitochondrial energy metabolism. Therefore, promoting mitophagy may become a potential therapeutic strategy for PD. Exercise, as a non-pharmacological intervention for PD, shows unique potential in improving PD symptoms and delaying disease progression, and the mechanism may be through promoting mitophagy, thereby promoting the clearance of damaged mitochondria, maintaining mitochondrial proteostasis, and ultimately relieving DA neuron degeneration and improving PD behavioral dysfunction. Therefore, this article reviews the role of mitophagy in the pathogenesis of PD and the prevention and treatment of mitophagy-mediated PD exercise.
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