背景 泛素-蛋白酶体途径介导的蛋白质翻译后修饰在调控正常细胞稳态和存活过程中发挥重要作用，脑缺血再灌注损伤过程中伴随着泛素蛋白酶体系统结构和功能的异常，脑缺血再灌注损伤后泛素化蛋白质修饰是当前研究的热点且存在较多争议。 目的 对脑缺血再灌注损伤后泛素化蛋白质修饰的研究进展和争议做一简要总结。 内容 分别综述泛素化蛋白质修饰在体内外脑缺血再灌注损伤过程中的作用，泛素化蛋白质修饰与谷氨酸兴奋性毒性损伤和脑缺血耐受以及SUMO化（Small Ubiquitin-like Modifier，SUMO）修饰在脑缺血再灌注损伤中的作用。 趋向 研究并阐明脑缺血再灌注损伤后泛素化蛋白质修饰的病理生理机制，可能为防治脑缺血再灌注损伤提供新思路或新策略。
Background Post-translational protein modification mediated by ubiquitin proteasome system (UPS) plays an important role in regulating normal cell homeostasis and cell survival. The structure and function of UPS changed abnormally during the process of cerebral ischemia-reperfusion injury. Ubiquitinated protein modification after cerebral ischemia-reperfusion injury is a hot topic in current research and there are many controversies. Objective To briefly summarize the research progress and controversy of ubiquitinated protein modification after cerebral ischemia-reperfusion. Content The role of ubiquitinated protein modification in cerebral ischemia-reperfusion injury model both in vitro and in vivo, the role of ubiquitinated protein modification in glutamate excitotoxicity, cerebral ischemic-tolerance were described separately and SUMOylation in cerebral ischemia-reperfusion injury was also sumarized. Trend Elucidating the pathophysiological mechanism of ubiquitinated protein modification after cerebral ischemia-reperfusion may provide new idea or strategy for prevention and treatment of cerebral ischemia-reperfusion injury.
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