文献类型：期刊文献

英文题名：Sestrin2 can alleviate endoplasmic reticulum stress to improve traumatic brain injury by activating AMPK/mTORC1 signaling pathway

作者：Zhou, Yu[1];Zhang, Yong[1];Botchway, Benson O. A.[2];Huang, Min[1];Liu, Xuehong[1]

机构：[1]Shaoxing Univ, Sch Med, Dept Histol & Embryol, Shaoxing 312000, Zhejiang, Peoples R China;[2]Bupa Cromwell Hosp, London, England

年份：2023

外文期刊名：METABOLIC BRAIN DISEASE

收录：SCI-EXPANDED(收录号：WOS:001112772500001)、、Scopus(收录号：2-s2.0-85178477181)、WOS

语种：英文

外文关键词：Injury; Neurological dysfunction; Mitochondrial dysfunction; Apoptosis; Inflammatory response

外文摘要：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.