Axonal degeneration in multiple sclerosis: the mitochondrial hypothesis.
Axonal degeneration in multiple sclerosis: the mitochondrial hypothesis.
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DOI：
10.1007/s11910-009-0060-3
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发表时间：
2009-09
影响因子：
5.6
通讯作者：
Forte, Michael
中科院分区：
文献类型：
--
作者：
Su, Kimmy G.;Banker, Gary;Bourdette, Dennis;Forte, Michael
多发性硬化症（MS）是一种中枢神经系统的慢性疾病，影响着全球超过200万人。传统上被认为是一种炎症性脱髓鞘疾病，最近的证据现在指出轴突变性对不可逆残疾的发展至关重要。研究表明，轴突变性发生在整个MS病程中。虽然引起轴突损伤的具体机制在不同阶段可能不同，但线粒体衰竭似乎是一个共同的潜在主题。这篇综述阐述了线粒体关于多发性硬化症轴突变性的假说，强调了线粒体功能障碍导致急性炎性病变轴突破坏和进行性多发性硬化症慢性轴突病的机制，重点将放在Ca2+、自由基产生和通透性过渡孔开放上，它们是线粒体衰竭、轴突运输损伤和随后的轴突变性的关键因素。此外，线粒体作为MS神经保护的治疗靶点的作用也将被讨论。
Multiple sclerosis (MS) is a chronic disease of the central nervous system, affecting upwards of 2 million people worldwide. Traditionally considered an inflammatory demyelinating disease, recent evidence now points to axonal degeneration as crucial to the development of irreversible disability. Studies show that axonal degeneration occurs throughout the entire MS disease course. While the specific mechanisms causing axonal damage may differ at various stages, mitochondrial failure seems to be a common underlying theme. This review addresses the mitochondrial hypothesis for axonal degeneration in MS, highlighting the mechanisms by which mitochondrial dysfunction leads to axonal disruption in acute inflammatory lesions and the chronic axonopathy in progressive MS. Emphasis will be placed on Ca2+, free radical production, and permeability transition pore opening as key players in mitochondrial failure, axonal transport impairment, and subsequent axonal degeneration. In addition, the role of mitochondria as therapeutic targets for neuroprotection in MS will be addressed.
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