Ferroptosis: a critical player and potential therapeutic target in traumatic brain injury and spinal cord injury

被引:56
作者
Li, Qing-Sheng [1 ,2 ]
Jia, Yan-Jie [1 ]
机构
[1] Zhengzhou Univ, Affiliated Hosp 1, Dept Neurol, Zhengzhou, Henan, Peoples R China
[2] Zhengzhou Univ, Acad Med Sci, Zhengzhou, Henan, Peoples R China
基金
中国国家自然科学基金;
关键词
ferroptosis; immune response; inflammation; iron homeostasis; lipid metabolism; medicine; programmed cell death; spinal cord injury; traumatic brain injury; IRON ACCUMULATION; PEROXIDATION; LIPROXSTATIN-1; POLARIZATION; SUPPRESSION; SENSITIVITY; INHIBITION; MECHANISM; RECEPTOR; PROTECTS;
D O I
10.4103/1673-5374.350187
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Ferroptosis, a new non-necrotizing programmed cell death (PCD), is driven by iron-dependent phospholipid peroxidation. Ferroptosis plays a key role in secondary traumatic brain injury and secondary spinal cord injury and is closely related to inflammation, immunity, and chronic injuries. The inhibitors against ferroptosis effectively improve iron homeostasis, lipid metabolism, redox stabilization, neuronal remodeling, and functional recovery after trauma. In this review, we elaborate on the latest molecular mechanisms of ferroptosis, emphasize its role in secondary central nervous trauma, and update the medicines used to suppress ferroptosis following injuries.
引用
收藏
页码:506 / 512
页数:7
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