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Targeting mitochondria-regulated ferroptosis: A new frontier in Parkinson's disease therapy

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机构: [1]Institute for Cancer Medicine and School of Basic Medical Sciences, Southwest Medical University, Luzhou, Sichuan, 646000, China [2]Department of Medical Microbiology, PGIMER, Chandigarh, 160012, India [3]Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Southwest Medical University, Luzhou, 646000, China [4]Department of Pediatrics, Birth Defects and Childhood Hematological Oncology Laboratory, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China [5]The Zigong Affiliated of Hospital of Southwest Medical University, Zigong mental health Center, Zigong Institute of Brain Science, Zigong, Sichuan Province, 643020, China [6]Health Science Center, Xi’an Jiaotong University, 710061, China
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关键词: Parkinson’s disease Reactive oxygen species Ferroptosis Mitochondria

摘要:
Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons in the substantial nigra. Mitochondrial dysfunction and mitochondrial oxidative stress are central to the pathogenesis of PD, with recent evidence highlighting the role of ferroptosis - a type of regulated cell death dependent on iron metabolism and lipid peroxidation. Mitochondria, the central organelles for cellular energy metabolism, play a pivotal role in PD pathogenesis through the production of Reactive oxygen species (ROS) and the disruption of iron homeostasis. This review explores the intricate interplay between mitochondrial dysfunction and ferroptosis in PD, focusing on key processes such as impaired electron transport chain function, tricarboxylic acid (TCA) cycle dysregulation, disruption of iron metabolism, and altered lipid peroxidation. We discuss key pathways, including the role of glutathione (GSH), mitochondrial ferritin, and the regulation of the mitochondrial labile iron pool (mLIP), which collectively influence the susceptibility of neurons to ferroptosis. Furthermore, this review emphasizes the importance of mitochondrial quality control mechanisms, such as mitophagy and mitochondrial biogenesis, in mitigating ferroptosis-induced neuronal death. Understanding these mechanisms linking the interplay between mitochondrial dysfunction and ferroptosis may pave the way for novel therapeutic approaches aimed at preserving mitochondrial integrity and preventing neuronal loss in PD.Copyright © 2025 The Authors. Published by Elsevier Ltd.. All rights reserved.

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出版当年[2025]版:
大类 | 2 区 医学
小类 | 2 区 药学 3 区 神经科学
最新[2025]版:
大类 | 2 区 医学
小类 | 2 区 药学 3 区 神经科学
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第一作者机构: [1]Institute for Cancer Medicine and School of Basic Medical Sciences, Southwest Medical University, Luzhou, Sichuan, 646000, China [3]Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Southwest Medical University, Luzhou, 646000, China
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通讯机构: [1]Institute for Cancer Medicine and School of Basic Medical Sciences, Southwest Medical University, Luzhou, Sichuan, 646000, China [5]The Zigong Affiliated of Hospital of Southwest Medical University, Zigong mental health Center, Zigong Institute of Brain Science, Zigong, Sichuan Province, 643020, China [6]Health Science Center, Xi’an Jiaotong University, 710061, China
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