Neurophysiology Unit, Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.
Department of Oral Biology and Diagnostic Sciences, Faculty of Dentistry, Chiang Mai University, Chiang Mai, Thailand.
Int J Neurosci. 2021 Oct;131(10):1019-1041. doi: 10.1080/00207454.2020.1765777. Epub 2020 May 14.
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.
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.
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.
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.
本综述旨在呈现和讨论线粒体功能障碍与几种神经病变模型（包括创伤诱导、化疗诱导、糖尿病诱导和 HIV 相关感觉神经病）之间关联的一致和不一致证据。
本综述的检索策略和纳入标准均为截至 2019 年 7 月之前在 PubMed 数据库中发表的所有研究文章。我们使用了“mitochondria”和“neuropathy”这两个术语来进行本次综述，且排除了非英文文章。
创伤、化疗药物、高血糖和 HIV 感染导致的线粒体损伤被广泛认为在神经病变发病机制中发挥重要作用。已经提出了几种线粒体损伤的机制。
线粒体的损伤导致细胞凋亡，这似乎是神经病变发病机制中的关键因素之一。针对线粒体的新型治疗策略可能是神经病变的潜在治疗靶点。
