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Possible roles of mitochondrial dysfunction in neuropathy
International Journal of Neuroscience ( IF 2.2 ) Pub Date : 2020-05-14 , DOI: 10.1080/00207454.2020.1765777
Chutikorn Khuankaew 1, 2, 3 , Passakorn Sawaddiruk 1, 4 , Poomarin Surinkaew 1, 5 , Nipon Chattipakorn 1, 6 , Siriporn C Chattipakorn 1, 2
Affiliation  

Abstract

Objectives

The present review aims to present and discuss the consistent and inconsistent evidence regarding the associations between mitochondrial dysfunction and several neuropathic models, including trauma-induced, chemotherapy-induced, diabetes-induced and HIV-associated sensory neuropathy.

Methods

The searching strategy and inclusion criteria for this review are all research articles in the PubMed database published before July 2019. We used the search terms ‘mitochondria’ and ‘neuropathy’ for the present review and non-English articles were excluded.

Results

Damage to mitochondria via trauma, chemotherapy drugs, hyperglycaemia and HIV infection has been widely discussed to play an important role in the pathogenesis of neuropathy. Several mechanisms of mitochondrial damages have been proposed.

Conclusion

The damage of mitochondria results in cellular apoptosis, which appears to be one of the key factors in the pathogenesis of neuropathy. Novel therapeutic strategies targeting mitochondria could be a potential therapeutic target in neuropathy.



中文翻译:

线粒体功能障碍在神经病变中的可能作用

摘要

目标

本综述旨在呈现和讨论关于线粒体功能障碍与几种神经病模型之间关联的一致和不一致的证据,包括创伤诱导、化疗诱导、糖尿病诱导和 HIV 相关的感觉神经病变。

方法

本综述的搜索策略和纳入标准均为 2019 年 7 月之前发表的 PubMed 数据库中的所有研究文章。我们在本综述中使用了搜索词“线粒体”和“神经病”,并排除了非英文文章。

结果

外伤、化疗药物、高血糖和 HIV 感染对线粒体的损​​伤已被广泛讨论,它们在神经病变的发病机制中起重要作用。已经提出了几种线粒体损伤机制。

结论

线粒体的损​​伤导致细胞凋亡,这似乎是神经病变发病机制的关键因素之一。针对线粒体的新治疗策略可能是神经病变的潜在治疗靶点。

更新日期:2020-05-14
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