Analysis of significance of mitochondrial dysfunction in the pathogenesis of diseases of the central nervous system

Q4 Neuroscience
O. P. Sokolik, G. Prozorova
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引用次数: 0

Abstract

One of the promising therapy areas for many diseases of the central nervous system is the search for agents of selective effect on mitochondria. Both the mitochondria themselves and the mitochondrial metabolism of the transformed cell of the central nervous system and activation of energy metabolism by reprogrammed mitochondria give impetus for the development of mitochondrial pharmacology to use the special properties of transformed cells mitochondria as targets for neuroprotective and neuroplastic effects. In this review, we analyse literary sources of domestic and foreign authors about the influence of mitochondrial dysfunction on various links in the pathogenesis of central nervous system diseases. Based on currently available data, scientists divided all signs of mitochondrial dysfunction in schizophrenia into three groups: morphological disorders of mitochondria, signs of a violation of the oxidative phosphorylation system and dysregulation of genes responsible for mitochondrial proteins. The therapeutic effect of drugs for central nervous system disorders should focus on reducing the accumulation of metabolic products and tissue breakdown, restoring mitochondrial functions and synaptic plasticity, and protecting mitochondria from toxic effects, thereby alleviating cognitive disorders with a neuroprotective effect.
线粒体功能障碍在中枢神经系统疾病发病机制中的意义分析
对许多中枢神经系统疾病的有前途的治疗领域之一是寻找对线粒体有选择性作用的药物。无论是线粒体本身,还是中枢神经系统转化细胞的线粒体代谢和重编程线粒体激活能量代谢,都推动了线粒体药理学的发展,利用转化细胞线粒体的特殊性质作为神经保护和神经可塑性作用的靶点。本文综述了线粒体功能障碍对中枢神经系统疾病发病各环节影响的国内外文献来源。根据现有的数据,科学家们将精神分裂症中所有线粒体功能障碍的迹象分为三组:线粒体形态障碍、氧化磷酸化系统破坏的迹象和负责线粒体蛋白质的基因失调。中枢神经系统疾病药物的治疗作用应侧重于减少代谢产物的积累和组织破坏,恢复线粒体功能和突触可塑性,保护线粒体免受毒性作用,从而减轻具有神经保护作用的认知障碍。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Neuroscience Research Notes
Neuroscience Research Notes Neuroscience-Neurology
CiteScore
1.00
自引率
0.00%
发文量
21
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