天津中医药大学学报2026，Vol.45Issue(1)：110-118,9.DOI:10.11656/j.issn.1673-9043.2026.01.15
PINK1/Parkin信号通路介导线粒体自噬在中西医防治帕金森病中的研究进展
Research progress on PINK1/Parkin pathway-mediated mitophagy in the prevention and treatment of Parkinson's disease with integrated Chinese and Western medicine
摘要
Abstract
Parkinson's disease(PD)is a common neurodegenerative disorder with a complex pathogenesis.Current clinical treatments have limited efficacy,making it difficult to effectively control disease progression.Mitochondrial dysfunction is a key factor leading to neuronal damage,and the imbalance of mitochondrial homeostasis is a crucial link in triggering mitochondrial dysfunction.The occurrence and development of PD are often accompanied by the disruption of mitochondrial homeostasis in neurons.Mitophagy,as a core mechanism regulating mitochondrial homeostasis,is of great significance for the prevention and treatment of PD.The PTEN-induced putative kinase 1(PINK1)/Parkin pathway is one of the classical pathways regulating mitophagy.Currently,studies have found that certain drugs and acupuncture treatments for PD can exert neuroprotective effects by modulating the PINK1/Parkin signaling pathway to target and improve neuronal mitochondrial homeostasis.In particular,the intervention of traditional Chinese medicine in regulating PINK1/Parkin pathway-mediated mitophagy for PD has attracted much attention.The article reviews the impact of PINK1/Parkin-mediated mitophagy on PD from the perspective of the PINK1/Parkin pathway and explores the therapeutic effects of both Chinese and Western medicine on PD by regulating this pathway,aiming to provide new research insights for the prevention and treatment of PD with integrated Chinese and Western medicine.关键词
中西医/帕金森病/PTEN诱导的假定激酶1/帕金蛋白/作用机制/研究进展Key words
integrated Chinese and Western medicine/Parkinson's disease/PINK1/Parkin/mechanism of action/research progress分类
医药卫生引用本文复制引用
刘馨,李威,杜宇征,张丽丽,王冰,曹蕊,郑高晗..PINK1/Parkin信号通路介导线粒体自噬在中西医防治帕金森病中的研究进展[J].天津中医药大学学报,2026,45(1):110-118,9.基金项目
国家重点研发计划项目(2019YFC0840709). （2019YFC0840709）
