粒体自噬
氧化应激
神经退行性变
活性氧
帕金森病
神经科学
自噬
疾病
生物
细胞生物学
医学
生物化学
内科学
细胞凋亡
作者
Bin Xiao,Joshua Kuruvilla,Eng‐King Tan
出处
期刊:npj Parkinson's disease
日期:2022-10-18
卷期号:8 (1)
被引量:37
标识
DOI:10.1038/s41531-022-00402-y
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.
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