Ng Gavin Yong-Quan, Lim Yun-An, Sobey Christopher G, Dheen Thameem, Fann David Yang-Wei, Arumugam Thiruma V
Department of Physiology, Yong Loo Lin School Medicine, National University of Singapore, Singapore.
Department of Physiology, Anatomy and Microbiology, School of Life Sciences, La Trobe University, Bundoora, Australia.
Ther Adv Neurol Disord. 2018 Apr 26;11:1756286418771815. doi: 10.1177/1756286418771815. eCollection 2018.
Despite extensive research, treatments for clinical stroke are still limited only to the administration of tissue plasminogen activator and the recent introduction of mechanical thrombectomy, which can be used in only a limited proportion of patients due to time constraints. A plethora of inflammatory events occur during stroke, arising in part due to the body's immune response to brain injury. Neuroinflammation contributes significantly to neuronal cell death and the development of functional impairment and death in stroke patients. Therefore, elucidating the molecular and cellular mechanisms underlying inflammatory damage following stroke injury will be essential for the development of useful therapies. Research findings increasingly point to the likelihood that epigenetic mechanisms play a role in the pathophysiology of stroke. Epigenetics involves the differential regulation of gene expression, including those involved in brain inflammation and remodelling after stroke. Hence, it is conceivable that epigenetic mechanisms may contribute to differential interindividual vulnerability and injury responses to cerebral ischaemia. In this review, we summarize recent findings on the emerging role of epigenetics in the regulation of neuroinflammation in stroke. We also discuss potential epigenetic targets that may be assessed for the development of stroke therapies.
尽管进行了广泛的研究，但临床中风的治疗方法仍然仅限于使用组织纤溶酶原激活剂以及最近引入的机械取栓术，由于时间限制，这些方法仅能应用于有限比例的患者。中风期间会发生大量炎症事件，部分原因是机体对脑损伤的免疫反应。神经炎症在很大程度上导致中风患者神经元细胞死亡以及功能障碍和死亡的发生。因此，阐明中风损伤后炎症损伤的分子和细胞机制对于开发有效的治疗方法至关重要。研究结果越来越多地表明，表观遗传机制可能在中风的病理生理学中发挥作用。表观遗传学涉及基因表达的差异调节，包括中风后参与脑部炎症和重塑的基因。因此，可以想象表观遗传机制可能导致个体间对脑缺血的易感性和损伤反应存在差异。在这篇综述中，我们总结了表观遗传学在中风神经炎症调节中新兴作用的最新研究结果。我们还讨论了可能用于评估中风治疗方法开发的潜在表观遗传靶点。
