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线粒体功能障碍导致多发性硬化症的神经退行性变。

Mitochondrial dysfunction contributes to neurodegeneration in multiple sclerosis.

机构信息

Department of Molecular Cell Biology and Immunology, VU University Medical Center, 1081BT, Amsterdam, The Netherlands.

Centre for Neuroregeneration, University of Edinburgh, Edinburgh, UK.

出版信息

Trends Mol Med. 2014 Mar;20(3):179-87. doi: 10.1016/j.molmed.2013.11.007. Epub 2013 Dec 24.

Abstract

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system. Current treatments are very effective in reducing the neuroinflammatory attack, but fail to significantly halt disease progression and associated loss of neuronal tissue. In recent years, it has become increasingly clear that dysfunctional mitochondria are important contributors to damage and loss of both axons and neurons. Observations in animal and histopathological studies suggest that infiltrating leukocytes and activated microglia play a central role in neuronal mitochondrial dysfunction. This review provides a comprehensive overview on the current knowledge regarding mitochondrial dysfunction in MS. Importantly, more insight into the cause and consequences of impaired mitochondrial function provide a basis for mitochondrial-targeted medicine to combat progressive MS.

摘要

多发性硬化症(MS)是一种中枢神经系统的炎症性脱髓鞘疾病。目前的治疗方法非常有效地减少神经炎症攻击,但未能显著阻止疾病进展和相关的神经元组织损失。近年来,越来越明显的是,功能失调的线粒体是导致轴突和神经元损伤和丢失的重要因素。动物和组织病理学研究的观察结果表明,浸润的白细胞和激活的小胶质细胞在神经元线粒体功能障碍中起核心作用。这篇综述提供了一个关于 MS 中线粒体功能障碍的综合概述。重要的是,对线粒体功能受损的原因和后果的更多了解为针对进行性 MS 的线粒体靶向药物治疗提供了基础。

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