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细胞内膜网膜应激和未展开的蛋白质反应:创伤性脑损伤进展中的新兴调节者

Yayi Yang^1,2, Dengfeng Lu¹, Menghan Wang^1,2

¹Department of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, 188Shizi Street, Suzhou, 215006, Jiangsu Province, China.

Cell death & disease

|February 20, 2024

概括

细胞内膜网膜应激 (ERS) 在创伤性脑损伤 (TBI) 中发挥双重作用,通过影响细胞生存途径. 了解ERS机制对于开发新的TBI治疗至关重要.

科学领域:

神经科学是一个神经科学.
细胞生物学细胞生物学
病理生理学病理生理学

背景情况:

创伤性脑损伤 (TBI) 是全球死亡和残疾的主要原因.
目前的TBI管理策略仍然不足,需要对疾病机制进行更深入的研究.
细胞内膜网膜应激 (ERS) 已成为中枢神经系统 (CNS) 疾病 (包括TBI) 的重要因素.

研究的目的:

在创伤性脑损伤 (TBI) 的背景下,审查细胞内膜网膜应激 (ERS) 的双重影响.
阐明关联ERS与TBI进展的潜在病理生理机制.
探索ERS作为TBI管理的潜在治疗目标.

主要方法:

文献综述侧重于内质网膜应激 (ERS) 和创伤性脑损伤 (TBI).
在TBI中分析未折叠蛋白质响应 (UPR) 途径 (PERK,IRE1,ATF6).
检查ESR和其他涉及二次TBI的分子途径之间的交叉声.

主要成果:

在TBI之后,ERS是由未折叠蛋白质的积累引起的,从而触发了UPR.
该UPR涉及三个关键路径:PERK,IRE1和ATF6,这些路径决定了细胞命运.
在TBI中,ERS表现出双重效应,可能有助于细胞存活和死亡.

结论:

细胞内膜网膜应激 (ERS) 与TBI中二次损伤进展密切相关.
ERS与线粒体功能障碍,氧化应激,神经炎症,自和细胞死亡途径相互作用.
准ERS是一个有希望的治疗途径,可以改善TBI的结果.

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