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金属离子内稳态受损与神经元线粒体功能障碍的关联。

Link of impaired metal ion homeostasis to mitochondrial dysfunction in neurons.

机构信息

Department of Chemistry, Ulsan National Institute of Science and Technology (UNIST), Ulsan 44919, Republic of Korea.

Department of Chemistry, Ulsan National Institute of Science and Technology (UNIST), Ulsan 44919, Republic of Korea.

出版信息

Curr Opin Chem Biol. 2018 Apr;43:8-14. doi: 10.1016/j.cbpa.2017.09.009. Epub 2017 Oct 28.

DOI:10.1016/j.cbpa.2017.09.009
PMID:29100100
Abstract

Manganese, iron, copper, and zinc are observed to play essential roles in mitochondria. The overload and depletion of metal ions in mitochondria under pathological conditions, however, could disturb mitochondrial compartments and functions leading to cell death. In this review, we mainly summarize how impaired metal ion homeostasis affects mitochondrial systems, such as membrane potentials, the tricarboxylic acid cycle, oxidative phosphorylation, and glutathione metabolism. In addition, based on current findings, we briefly describe a recent understanding of the relationship among metal ion dysregulation, mitochondrial dysfunction, and the pathogeneses of neurodegenerative diseases.

摘要

锰、铁、铜和锌被观察到在线粒体中发挥重要作用。然而,在病理条件下,线粒体中金属离子的超载和耗竭会扰乱线粒体区室和功能,导致细胞死亡。在这篇综述中,我们主要总结了金属离子稳态失衡如何影响线粒体系统,如膜电位、三羧酸循环、氧化磷酸化和谷胱甘肽代谢。此外,基于目前的发现,我们简要描述了对金属离子失调、线粒体功能障碍与神经退行性疾病发病机制之间关系的最新认识。

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