Mitochondrial dysfunction and neurodegeneration in multiple sclerosis.
Mitochondrial dysfunction and neurodegeneration in multiple sclerosis.
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DOI：
10.3389/fphys.2013.00169
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发表时间：
2013
影响因子：
4
通讯作者：
Forte M
中科院分区：
文献类型：
--
作者：
Su K;Bourdette D;Forte M
多发性硬化症（MS）传统上被认为是一种自身免疫性炎症性疾病，会导致脱髓鞘和临床衰弱，我们目前的标准抗炎和免疫抑制治疗方案就证明了这一点。虽然这些方法确实控制了临床复发的频率，但它们并不能阻止困扰许多多发性硬化症患者的进行性功能衰退。许多研究表明，神经退行性过程也可能在疾病早期阶段的多发性硬化症中发挥重要作用，目前的假设之一认为线粒体功能障碍是一个关键的促进机制。我们假设活性氧（ROS）和钙失调介导的病理性通透性转换孔（PTP）开放是多发性硬化症线粒体功能障碍和神经变性的核心。这篇重点综述强调了支持这一假设的最新证据，特别强调了我们对线粒体靶向氧化还原酶 p66ShcA 的体外和体内工作。
Multiple sclerosis (MS) has traditionally been considered an autoimmune inflammatory disorder leading to demyelination and clinical debilitation as evidenced by our current standard anti-inflammatory and immunosuppressive treatment regimens. While these approaches do control the frequency of clinical relapses, they do not prevent the progressive functional decline that plagues many people with MS. Many avenues of research indicate that a neurodegenerative process may also play a significant role in MS from the early stages of disease, and one of the current hypotheses identifies mitochondrial dysfunction as a key contributing mechanism. We have hypothesized that pathological permeability transition pore (PTP) opening mediated by reactive oxygen species (ROS) and calcium dysregulation is central to mitochondrial dysfunction and neurodegeneration in MS. This focused review highlights recent evidence supporting this hypothesis, with particular emphasis on our in vitro and in vivo work with the mitochondria-targeted redox enzyme p66ShcA.
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