Emerging Role for Methylation in Multiple Sclerosis: Beyond DNA.
Emerging Role for Methylation in Multiple Sclerosis: Beyond DNA.
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DOI：
10.1016/j.molmed.2017.04.004
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发表时间：
2017-06
影响因子：
13.6
通讯作者：
Guerau-de-Arellano M
中科院分区：
文献类型：
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作者：
Webb LM;Guerau-de-Arellano M
多发性硬化（MS）是中枢神经系统的慢性炎症性疾病。驱动MS的炎症和神经退行性途径受到DNA、赖氨酸和精氨酸甲基化的调节，如通过用于甲基化检测或功能丧失的新工具所进行的研究所证明的。在这里，我们提出的证据表明，MS与影响甲基化的遗传变异和代谢变化有关。此外，我们全面回顾了目前对甲基化如何影响CNS恢复力和神经再生潜力以及炎症与调节性T辅助细胞平衡的理解。这些研究结果在MS的治疗相关性的背景下进行了讨论，在其他神经和免疫介导的疾病中具有广泛的意义。
Multiple Sclerosis (MS) is a chronic inflammatory disease of the central nervous system. The inflammatory and neurodegenerative pathways driving MS are modulated by DNA, lysine and arginine methylation, as evidenced by studies made possible by novel tools for methylation detection or loss-of-function. Here, we present evidence that MS is associated with genetic variants and metabolic changes that impact methylation. Further, we comprehensively review the current understanding of how methylation can impact CNS resilience and neuroregenerative potential, as well as inflammatory vs. regulatory T helper-cell balance. These findings are discussed in the context of therapeutic relevance for MS, with broad implications in other neurologic and immune-mediated diseases.