解读DNA甲基化在多发性硬化症中的作用:新出现的问题。

Q1 Medicine
Auto-Immunity Highlights Pub Date : 2016-12-01 Epub Date: 2016-09-07 DOI:10.1007/s13317-016-0084-z
Maria Sokratous, Efthimios Dardiotis, Zisis Tsouris, Eleni Bellou, Amalia Michalopoulou, Vasileios Siokas, Stylianos Arseniou, Tzeni Stamati, Georgios Tsivgoulis, Dimitrios Bogdanos, Georgios M Hadjigeorgiou
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引用次数: 23

摘要

多发性硬化症(MS)是一种中枢神经系统的自身免疫性炎症和神经退行性疾病,涉及几种尚未完全阐明的病理生理机制。越来越多的证据表明,DNA碱基、组蛋白和微rna水平的表观遗传修饰可能会增加多发性硬化症的风险。DNA甲基化似乎在多发性硬化症的表观遗传学中起着重要作用,因为基因组启动子区域的异常甲基化可能是多发性硬化症发生和发展的几个过程的基础。在本文中,我们讨论了目前对DNA甲基化在多发性硬化症中作用的理解。可能的治疗意义和未来出现的问题。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Deciphering the role of DNA methylation in multiple sclerosis: emerging issues.

Multiple sclerosis (MS) is an autoimmune inflammatory and neurodegenerative disease of the central nervous system that involves several not yet fully elucidated pathophysiologic mechanisms. There is increasing evidence that epigenetic modifications at level of DNA bases, histones, and micro-RNAs may confer risk for MS. DNA methylation seems to have a prominent role in the epigenetics of MS, as aberrant methylation in the promoter regions across genome may underlie several processes involved in the initiation and development of MS. In the present review, we discuss current understanding regarding the role of DNA methylation in MS, possible therapeutic implications and future emerging issues.

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