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线粒体在多发性硬化症中的作用。

Role of mitochondria in multiple sclerosis.

作者信息

Kalman Bernadette

机构信息

Department of Neurology, Saint Luke's Roosevelt Hospital Center, Columbia University, 432 West 58th Street, Room 226, New York, NY 10019, USA.

出版信息

Curr Neurol Neurosci Rep. 2006 May;6(3):244-52. doi: 10.1007/s11910-006-0012-0.

DOI:10.1007/s11910-006-0012-0
PMID:16635434
Abstract

This review presents inherited and acquired forms of mitochondrial dysfunction associated with oligodendrocytopathy and neurodegeneration in order to better understand the degenerative features of inflammatory demyelination. The recognition that various mitochondrial mechanisms are involved in the pathogenesis of multiple sclerosis leads to therapeutic considerations, re-emphasizing the importance of early neuroprotection in combination with the approved means of immune modulation.

摘要

本综述介绍了与少突胶质细胞病变和神经退行性变相关的线粒体功能障碍的遗传和获得性形式,以便更好地理解炎性脱髓鞘的退行性特征。认识到多种线粒体机制参与多发性硬化症的发病机制引发了治疗方面的考虑,再次强调了早期神经保护与已批准的免疫调节方法相结合的重要性。

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本文引用的文献

1
Mitochondrial dysfunction as a cause of axonal degeneration in multiple sclerosis patients.线粒体功能障碍作为多发性硬化症患者轴突变性的一个原因。
Ann Neurol. 2006 Mar;59(3):478-89. doi: 10.1002/ana.20736.
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Severe impairment of complex I-driven adenosine triphosphate synthesis in leber hereditary optic neuropathy cybrids.莱伯遗传性视神经病变胞质杂种中复合体I驱动的三磷酸腺苷合成的严重受损
Arch Neurol. 2005 May;62(5):730-6. doi: 10.1001/archneur.62.5.730.
3
Mitochondrial encephalomyopathies: an update.线粒体脑肌病:最新进展
NADH-dehydrogenase type-2 suppresses irreversible visual loss and neurodegeneration in the EAE animal model of MS.
NADH 脱氢酶-2 可抑制多发性硬化症 EAE 动物模型中的不可逆视力丧失和神经退行性变。
Mol Ther. 2013 Oct;21(10):1876-88. doi: 10.1038/mt.2013.104. Epub 2013 Jun 11.
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MRI characteristics of patients with antiphospholipid syndrome and multiple sclerosis.抗磷脂综合征与多发性硬化症患者的 MRI 特征。
J Neurol. 2010 Jan;257(1):63-71. doi: 10.1007/s00415-009-5264-6. Epub 2009 Jul 26.
5
Mitochondrial DNA haplogroup T is associated with coronary artery disease and diabetic retinopathy: a case control study.线粒体DNA单倍群T与冠状动脉疾病和糖尿病视网膜病变相关:一项病例对照研究。
BMC Med Genet. 2009 Apr 21;10:35. doi: 10.1186/1471-2350-10-35.
6
Dissecting the effects of mtDNA variations on complex traits using mouse conplastic strains.利用小鼠同核异质系剖析线粒体DNA变异对复杂性状的影响。
Genome Res. 2009 Jan;19(1):159-65. doi: 10.1101/gr.078865.108. Epub 2008 Nov 26.
7
Association of common mitochondrial DNA variants with multiple sclerosis and systemic lupus erythematosus.常见线粒体DNA变异与多发性硬化症和系统性红斑狼疮的关联。
Clin Immunol. 2008 Oct;129(1):31-5. doi: 10.1016/j.clim.2008.07.011. Epub 2008 Aug 16.
8
Lack of mitochondrial DNA deletions in lesions of multiple sclerosis.多发性硬化症病变中不存在线粒体DNA缺失。
Neuromolecular Med. 2008;10(3):187-94. doi: 10.1007/s12017-008-8025-2.
Neuromuscul Disord. 2005 Apr;15(4):276-86. doi: 10.1016/j.nmd.2004.12.008.
4
Tissue preconditioning may explain concentric lesions in Baló's type of multiple sclerosis.组织预处理可能解释巴洛型多发性硬化症中的同心圆状病变。
Brain. 2005 May;128(Pt 5):979-87. doi: 10.1093/brain/awh457. Epub 2005 Mar 17.
5
Mitochondrial dysfunction plays a key role in progressive axonal loss in Multiple Sclerosis.线粒体功能障碍在多发性硬化症的进行性轴突丧失中起关键作用。
Med Hypotheses. 2005;64(4):669-77. doi: 10.1016/j.mehy.2004.09.001.
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Mitochondrial damage and histotoxic hypoxia: a pathway of tissue injury in inflammatory brain disease?线粒体损伤与组织中毒性缺氧:炎症性脑病中的组织损伤途径?
Acta Neuropathol. 2005 Jan;109(1):49-55. doi: 10.1007/s00401-004-0954-8. Epub 2005 Jan 11.
7
Genetic variants of Complex I in multiple sclerosis.多发性硬化症中复合体I的基因变异
J Neurol Sci. 2005 Jan 15;228(1):55-64. doi: 10.1016/j.jns.2004.09.027.
8
Neuropathology of white matter disease in Leber's hereditary optic neuropathy.莱伯遗传性视神经病变中白质疾病的神经病理学
Brain. 2005 Jan;128(Pt 1):35-41. doi: 10.1093/brain/awh310. Epub 2004 Oct 13.
9
Molecular changes in neurons in multiple sclerosis: altered axonal expression of Nav1.2 and Nav1.6 sodium channels and Na+/Ca2+ exchanger.多发性硬化症中神经元的分子变化:Nav1.2和Nav1.6钠通道以及Na+/Ca2+交换器的轴突表达改变
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LEBER'S DISEASE WITH SYMPTOMS RESEMBLING DISSEMINATED SCLEROSIS.伴有类似播散性硬化症状的莱伯病。
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