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拓宽视野:铁死亡作为创伤性脑损伤的新靶点

Broadening horizons: ferroptosis as a new target for traumatic brain injury.

作者信息

Wei Ziqing, Yu Haihan, Zhao Huijuan, Wei Mingze, Xing Han, Pei Jinyan, Yang Yang, Ren Kaidi

机构信息

Department of Neurology, The First Affiliated Hospital of Zhengzhou University, No. 1, Jianshe East Road, Erqi District, Zhengzhou, China.

Henan Key Laboratory of Cerebrovascular Diseases, The First Affiliated Hospital of Zhengzhou University, No. 1, Jianshe East Road, Erqi District, Zhengzhou, China.

出版信息

Burns Trauma. 2024 Jan 18;12:tkad051. doi: 10.1093/burnst/tkad051. eCollection 2024.

Abstract

Traumatic brain injury (TBI) is a leading cause of death and disability worldwide, with ~50 million people experiencing TBI each year. Ferroptosis, a form of regulated cell death triggered by iron ion-catalyzed and reactive oxygen species-induced lipid peroxidation, has been identified as a potential contributor to traumatic central nervous system conditions, suggesting its involvement in the pathogenesis of TBI. Alterations in iron metabolism play a crucial role in secondary injury following TBI. This study aimed to explore the role of ferroptosis in TBI, focusing on iron metabolism disorders, lipid metabolism disorders and the regulatory axis of system Xc/glutathione/glutathione peroxidase 4 in TBI. Additionally, we examined the involvement of ferroptosis in the chronic TBI stage. Based on these findings, we discuss potential therapeutic interventions targeting ferroptosis after TBI. In conclusion, this review provides novel insights into the pathology of TBI and proposes potential therapeutic targets.

摘要

创伤性脑损伤(TBI)是全球范围内死亡和残疾的主要原因,每年约有5000万人发生TBI。铁死亡是一种由铁离子催化和活性氧诱导的脂质过氧化引发的程序性细胞死亡形式,已被确定为创伤性中枢神经系统疾病的潜在促成因素,提示其参与TBI的发病机制。铁代谢改变在TBI后的继发性损伤中起关键作用。本研究旨在探讨铁死亡在TBI中的作用,重点关注TBI中的铁代谢紊乱、脂质代谢紊乱以及系统Xc/谷胱甘肽/谷胱甘肽过氧化物酶4的调节轴。此外,我们研究了铁死亡在TBI慢性期的参与情况。基于这些发现,我们讨论了TBI后针对铁死亡的潜在治疗干预措施。总之,本综述为TBI的病理学提供了新的见解,并提出了潜在的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f77f/10799763/649a0ffe446f/tkad051f1.jpg

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