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.

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拓宽视野：铁死亡作为创伤性脑损伤的新靶标

创伤性脑损伤 (TBI) 是全球死亡和残疾的主要原因，每年约有 5000 万人经历 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受调节细胞死亡形式，已被确定为创伤性中枢神经系统疾病的潜在促成因素，表明其参与了 TBI 的发病机制。铁代谢的改变在 TBI 后的继发性损伤中起着至关重要的作用。本研究旨在探讨铁死亡在TBI中的作用，重点关注TBI中铁代谢紊乱、脂质代谢紊乱以及Xc−/谷胱甘肽/谷胱甘肽过氧化物酶4系统的调节轴。此外，我们还研究了铁死亡在慢性 TBI 阶段的参与情况。基于这些发现，我们讨论了针对 TBI 后铁死亡的潜在治疗干预措施。总之，这篇综述为 TBI 的病理学提供了新的见解，并提出了潜在的治疗靶点。