Mitophagy and reactive oxygen species interplay in Parkinson's disease

被引:36
|
作者
Xiao, Bin [1 ,2 ]
Kuruvilla, Joshua [3 ]
Tan, Eng-King [1 ,2 ,3 ]
机构
[1] Natl Neurosci Inst, Dept Neurol, Singapore, Singapore
[2] Duke NUS Med Sch, Neurosci Acad Clin Program, Singapore, Singapore
[3] Duke NUS Med Sch, Neurosci & Behav Disorders Program, Singapore, Singapore
基金
英国医学研究理事会;
关键词
OXIDATIVE STRESS; MITOCHONDRIAL DYSFUNCTION; DAMAGED MITOCHONDRIA; DOPAMINERGIC-NEURONS; LIPID-PEROXIDATION; ENDOTHELIAL-CELLS; UBIQUITIN CHAIN; IN-VIVO; PINK1; AUTOPHAGY;
D O I
10.1038/s41531-022-00402-y
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Mitophagy impairment and oxidative stress are cardinal pathological hallmarks in Parkinson's disease (PD), a common age-related neurodegenerative condition. The specific interactions between mitophagy and reactive oxygen species (ROS) have attracted considerable attention even though their exact interplay in PD has not been fully elucidated. We highlight the interactions between ROS and mitophagy, with a focus on the signalling pathways downstream to ROS that triggers mitophagy and draw attention to potential therapeutic compounds that target these pathways in both experimental and clinical models. Identifying a combination of ROS inhibitors and mitophagy activators to provide a physiologic balance in this complex signalling pathways may lead to a more optimal outcome. Deciphering the exact temporal relationship between mitophagy and oxidative stress and their triggers early in the course of neurodegeneration can unravel mechanistic clues that potentially lead to the development of compounds for clinical drug trials focusing on prodromic PD or at-risk individuals.
引用
收藏
页数:13
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