Research progress on the role of mitochondrial complex I in the pathogenesis of Parkinson's disease.
- Author:
Xiang YIN
1
;
Cheng SUN
1
Author Information
1. Key Laboratory for Neuroregeneration, Co-Innovation Center of Neuroregeneration, Nantong University, Nantong 226001, China.
- Publication Type:English Abstract
- MeSH:
Parkinson Disease/metabolism*;
Humans;
Electron Transport Complex I/metabolism*;
Mitochondria/physiology*;
Reactive Oxygen Species/metabolism*;
Dopaminergic Neurons/metabolism*;
Animals;
Adenosine Triphosphate/metabolism*
- From:
Acta Physiologica Sinica
2025;77(1):167-180
- CountryChina
- Language:Chinese
-
Abstract:
Currently, the incidence of Parkinson's disease (PD) is on the rise. More and more evidences suggest that mitochondrial dysfunction plays a crucial role in the etiology of PD, and dysfunction of mitochondrial complex I (MCI) is one of the most critical factors leading to mitochondrial dysfunction. On one hand, MCI dysfunction stimulates dopaminergic neurons to produce reactive oxygen species (ROS). On the other hand, MCI dysfunction decreases dopaminergic neuron viability and reduces ATP production. All these outcomes promote the pathological progression of PD. This review summarizes research progress on the role of MCI in the pathogenesis of PD, as well as PD treatment strategies based on MCI.
