Endoplasmic reticulum (ER) is the main organelle for protein synthesis, trafficking and maintaining intracellular Ca2+ homeostasis. The proportion of ischemic stroke in central nervous system diseases is increasing with each passing year, which is a prevalent reason of death and disability in the world. Cerebral ischemia causes several stress responses where ER in stress state initiates unfolded protein response (UPR) due to accumulation of misfolded and unfolded protein as well as Ca2 + overload, which is associated with a specialized set of inflammatory and apoptotic signaling pathways controlling the fate of nerve cells. Mild ER stress promotes cells to break away from danger signals and enter the adaptive procedure with the activation of pro-survival mechanism to rescue ischemic injury, while chronic ER stress generally serves as a detrimental role on nerve cells via triggering diverse pro-apoptotic mechanism. A reasonable understanding and exploration of the underlying molecular mechanism related to ER stress and cerebral ischema is a prerequisite for a major breakthrough in stroke treatment in the future. This review focuses on recent findings of the ER stress as well as the progress research of mechanism in ischemic stroke prognosis provide a new treatment idea for recovery of cerebral ischemia.

中文翻译：

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脑缺血内质网应激的机制

内质网 (ER) 是蛋白质合成、运输和维持细胞内 Ca2+ 稳态的主要细胞器。缺血性脑卒中在中枢神经系统疾病中的比例逐年增加，是世界上普遍存在的死亡和致残原因。脑缺血会导致几种应激反应，其中应激状态下的 ER 由于错误折叠和未折叠蛋白的积累以及 Ca2+ 超载而启动未折叠蛋白反应 (UPR)，这与控制命运的一组专门的炎症和凋亡信号通路有关。神经细胞。轻度内质网应激促使细胞脱离危险信号进入适应性过程，激活促生存机制以挽救缺血性损伤，而慢性内质网应激通常通过触发多种促凋亡机制对神经细胞产生有害作用。合理认识和探索与内质网应激和脑缺血相关的潜在分子机制，是未来脑卒中治疗取得重大突破的先决条件。本文就ER应激的最新发现以及缺血性脑卒中预后机制的研究进展进行综述，为脑缺血的恢复提供新的治疗思路。