Ischemic stroke is an acute cerebrovascular disease characterized by sudden interruption of blood flow in a certain part of the brain, leading to serious disability and death. At present, treatment methods for ischemic stroke are limited to thrombolysis or thrombus removal, but the treatment window is very narrow. However, recovery of cerebral blood circulation further causes cerebral ischemia/reperfusion injury (CIRI). The endoplasmic reticulum (ER) plays an important role in protein secretion, membrane protein folding, transportation, and maintenance of intracellular calcium homeostasis. Endoplasmic reticulum stress (ERS) plays a crucial role in cerebral ischemia pathophysiology. Mild ERS helps improve cell tolerance and restore cell homeostasis; however, excessive or long-term ERS causes apoptotic pathway activation. Specifically, the protein kinase R-like endoplasmic reticulum kinase (PERK), activating transcription factor 6 (ATF6), and inositol-requiring enzyme 1 (IRE1) pathways are significantly activated following initiation of the unfolded protein response (UPR). CIRI-induced apoptosis leads to nerve cell death, which ultimately aggravates neurological deficits in patients. Therefore, it is necessary and important to comprehensively explore the mechanism of ERS in CIRI to identify methods for preserving brain cells and neuronal function after ischemia.

缺血性中风是一种急性脑血管疾病，其特征是大脑某一部位的血流突然中断，导致严重的残疾和死亡。目前，缺血性脑卒中的治疗方法仅限于溶栓或血栓清除，但治疗窗非常窄。然而，脑血液循环的恢复进一步导致脑缺血/再灌注损伤（CIRI）。内质网 (ER) 在蛋白质分泌、膜蛋白折叠、运输和维持细胞内钙稳态中起重要作用。内质网应激（ERS）在脑缺血病理生理学中起着至关重要的作用。温和的 ERS ​​有助于提高细胞耐受性并恢复细胞稳态；然而，过度或长期 ERS ​​会导致凋亡通路激活。具体来说，蛋白激酶 R 样内质网激酶 (PERK)、激活转录因子 6 (ATF6) 和肌醇需要酶 1 (IRE1) 通路在展开蛋白反应 (UPR) 启动后显着激活。CIRI 诱导的细胞凋亡导致神经细胞死亡，最终加重患者的神经功能缺损。因此，全面探索 ERS ​​在 CIRI 中的作用机制，以确定缺血后脑细胞和神经元功能的保存方法是必要和重要的。这最终会加重患者的神经功能缺损。因此，全面探索 ERS ​​在 CIRI 中的作用机制，以确定缺血后脑细胞和神经元功能的保存方法是必要和重要的。这最终会加重患者的神经功能缺损。因此，全面探索 ERS ​​在 CIRI 中的作用机制，以确定缺血后脑细胞和神经元功能的保存方法是必要和重要的。