Traumatic brain injury (TBI), as a serious central nervous system disease, can result in severe neurological dysfunction or even disability and death of patients. The early and effective intervention of secondary brain injury can improve the prognosis of TBI. Endoplasmic reticulum (ER) stress is one of the main reasons to recover TBI. ER stress inhibition may be beneficial in treating TBI. Sestrin2 is a crucial regulator of ER stress, and its activation can significantly improve TBI. In this paper, we analyze the biological function of sestrin2, the latest findings on ER stress, and the relationship between ER stress and TBI. We elucidate the relationship of sestrin2 inhibiting ER stress via activating the AMP-activated protein kinase (AMPK)/mammalian target of rapamycin complex 1 (MTORC1) signaling. Finally, we elaborate on the possible role of sestrin2 in TBI and explain how its activation potentially improves TBI.

创伤性脑损伤（TBI）作为一种严重的中枢神经系统疾病，可导致患者严重的神经功能障碍甚至残疾和死亡。对继发性脑损伤的早期有效干预可以改善TBI的预后。内质网（ER）应激是TBI恢复的主要原因之一。内质网应激抑制可能有益于治疗 TBI。Sestrin2 是 ER 应激的重要调节因子，其激活可以显着改善 TBI。在本文中，我们分析了sestrin2的生物学功能、ER应激的最新发现以及ER应激与TBI的关系。我们阐明了 sestrin2 通过激活 AMP 激活蛋白激酶 (AMPK)/哺乳动物雷帕霉素靶复合物 1 (MTORC1) 信号传导抑制 ER 应激的关系。最后，我们详细阐述了 sestrin2 在 TBI 中的可能作用，并解释了它的激活如何潜在地改善 TBI。