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线粒体与神经炎症——多发性硬化症(MS)、莱伯遗传性视神经病变(LHON)和 LHON-MS。

Mitochondria in neuroinflammation - Multiple sclerosis (MS), leber hereditary optic neuropathy (LHON) and LHON-MS.

机构信息

Department of Clinical Neuroscience & MRC Mitochondrial Biology Unit, University of Cambridge, UK.

出版信息

Neurosci Lett. 2019 Sep 25;710:132932. doi: 10.1016/j.neulet.2017.06.051. Epub 2017 Jun 28.

DOI:10.1016/j.neulet.2017.06.051
PMID:28668384
Abstract

Mitochondrial dysfunction is associated with neuroinflammation and neurodegenerative disease, but its role as a driver in these processes is uncertain. Understanding the pathogenesis of inherited mitochondrial disorders may help us to uncover mechanisms involved during acquired mitochondrial dysfunction. We review the mechanisms of mitochondrial dysfunction in Leber's hereditary optic neuropathy and multiple sclerosis and discuss shared clinical and molecular features in both conditions. Targeting mitochondrial pathways involved in inflammation or apoptosis may be a possible therapeutic approach in multiple sclerosis.

摘要

线粒体功能障碍与神经炎症和神经退行性疾病有关,但它在这些过程中作为驱动因素的作用尚不确定。了解遗传性线粒体疾病的发病机制可能有助于我们揭示获得性线粒体功能障碍过程中涉及的机制。我们回顾了莱伯遗传性视神经病变和多发性硬化症中线粒体功能障碍的机制,并讨论了这两种疾病的共同临床和分子特征。靶向涉及炎症或细胞凋亡的线粒体途径可能是多发性硬化症的一种可行的治疗方法。

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