Chinese Journal of Tissue Engineering Research ›› 2025, Vol. 29 ›› Issue (17): 3668-3674.doi: 10.12307/2025.626

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Mechanism of alpha-synuclein in mitochondrial damage induced by Parkinson’s disease

Wang Jingying1, 2, Ren Binbin2, Ma Suna1, Yang Yueyue1, 2, Wu Song1, 2, Guan Mengya1, 2    

  1. 1School of Rehabilitation, Henan University of Chinese Medicine, Zhengzhou 450000, Henan Province, China; 2The First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou 450000, Henan Province, China
  • Received:2024-05-11 Accepted:2024-07-15 Online:2025-06-18 Published:2024-11-06
  • Contact: Ren Binbin, Chief physician, Master’s supervisor, The First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou 450000, Henan Province, China
  • About author:Wang Jingying, Master candidate, School of Rehabilitation, Henan University of Chinese Medicine, Zhengzhou 450000, Henan Province, China; The First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou 450000, Henan Province, China
  • Supported by:
    Traditional Chinese Medicine Inheritance and Innovation Talent Project (Zhongjing Project) (to RBB); 2022 Henan Province Chinese Medicine Top Talent Cultivation Program Special Project, No. 2022ZYBJ09 (to RBB) 

Abstract: BACKGROUND: Currently, the pathogenesis of Parkinson’s disease is not clear. Relevant studies have shown that α-synuclein and mitochondria are closely related to the pathogenesis of Parkinson’s disease. It mainly involves oxidative stress, mitochondrial complex damage, calcium homeostasis, mitochondrial dynamics and mitochondrial quality control.
OBJECTIVE: To review the association between α-synuclein and mitochondrial damage in Parkinson’s disease.
METHODS: The first author searched more than 50 documents from CNKI and WanFang databases from 2010 to 2024 using the keywords of “Parkinson’s disease, mitochondrial damage and mechanism, α-synuclein” in Chinese as well as more than 750 documents from PubMed between 2010 and 2024 using the keywords of “Parkinson’s disease, alpha-synuclein, mitochondria, oxidative stress, calcium homeostasis, mitophagy, mitochondrial dynamics, mitochondrial protein introduction” in English. Finally, 70 documents were included for review. 
RESULTS AND CONCLUSION: Recent studies have confirmed the important role of mitochondrial dysfunction in the pathophysiology of Parkinson’s disease, and the interaction between α-synuclein and mitochondria is a particularly significant factor in the pathogenesis of Parkinson’s disease. The cascade of events that begin with naturally unfolded α-synuclein and eventually form mature fibril is collectively known as α-synuclein aggregation. The toxicity of aggregation accumulates in dopaminergic neurons and then disrupts mitochondrial function, thereby triggering Parkinson’s disease. Therefore, the underlying mechanism of this bidirectional relationship between α-synuclein and mitochondrial dysfunction may provide new insights into the pathophysiology of Parkinson’s disease.

中国组织工程研究杂志出版内容重点:组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程

Key words: Parkinson’s disease, α-synuclein, mitochondria, oxidative stress, calcium, mitochondrial dynamics, mitochondrial autophagy, protein introduction mechanism

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