Oxidative stress, mitochondrial damage and neurodegenerative diseases.
Oxidative stress, mitochondrial damage and neurodegenerative diseases.
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DOI：
10.3969/j.issn.1673-5374.2013.21.009
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发表时间：
2013-07-25
影响因子：
6.1
通讯作者：
Zhang D
中科院分区：
文献类型：
--
作者：
Guo C;Sun L;Chen X;Zhang D
氧化应激和线粒体损伤与几种神经退行性疾病的发病机制有关，包括阿尔茨海默病、帕金森病和肌萎缩性侧索硬化症。氧化应激的特征是活性氧的过量产生，可诱导线粒体DNA突变，损伤线粒体呼吸链，改变膜通透性，影响Ca2+稳态和线粒体防御系统。所有这些变化都与这些神经退行性疾病的发展有关，介导或放大神经元功能障碍并引发神经变性。本文总结了氧化应激和线粒体损伤对神经退行性疾病发病的贡献，并讨论了改变线粒体功能障碍的策略，这些策略可能是治疗各种神经退行性疾病的有吸引力的治疗干预措施。
Oxidative stress and mitochondrial damage have been implicated in the pathogenesis of several neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis. Oxidative stress is characterized by the overproduction of reactive oxygen species, which can induce mitochondrial DNA mutations, damage the mitochondrial respiratory chain, alter membrane permeability, and influence Ca2+ homeostasis and mitochondrial defense systems. All these changes are implicated in the development of these neurodegenerative diseases, mediating or amplifying neuronal dysfunction and triggering neurodegeneration. This paper summarizes the contribution of oxidative stress and mitochondrial damage to the onset of neurodegenerative eases and discusses strategies to modify mitochondrial dysfunction that may be attractive therapeutic interventions for the treatment of various neurodegenerative diseases.
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