Targeting Ferroptosis Promotes Functional Recovery by Mitigating White Matter Injury Following Acute Carbon Monoxide Poisoning

被引：5

作者：

Wang, Shuhong ^{[1
]}

Xiong, Binyuan ^{[1
]}

Tian, Yin ^{[2
]}

Hu, Quan ^{[1
]}

Jiang, Xuheng ^{[1
]}

Zhang, Ji ^{[1
]}

Chen, Lin ^{[1
]}

Wang, Ruilie ^{[1
]}

Li, Mo ^{[1
]}

Zhou, Xin ^{[1
]}

Zhang, Tianxi ^{[1
]}

Ge, Hongfei ^{[1
]}

Yu, Anyong ^{[1
]}

机构：

[1] Zunyi Med Univ, Dept Emergency, Affiliated Hosp, Zunyi 563000, Guizhou, Peoples R China

[2] First Peoples Hosp Zunyi, Dept Cardiol, Zunyi 133012, Guizhou, Peoples R China

来源：

MOLECULAR NEUROBIOLOGY | 2024年 / 61卷 / 02期

基金：

中国国家自然科学基金;

关键词：

Acute carbon monoxide poisoning; White matter injury; Ferroptosis; Ferrostatin-1; Nrf2/HO-1 signaling pathway; DELAYED ENCEPHALOPATHY; HYPERBARIC-OXYGEN;

D O I：

10.1007/s12035-023-03603-5

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Survivors experiencing acute carbon monoxide poisoning (ACMP) tend to develop white matter injury (WMI). The mechanism of ACMP-induced WMI remains unclear. Considering the role of ferroptosis in initiating oligodendrocyte damage to deteriorate WMI, exploring therapeutic options to attenuate ferroptosis is a feasible approach to alleviating WMI. Our results indicated that ACMP induced accumulation of iron and reactive oxygen species (ROS) eventually leading to WMI and motor impairment after ACMP. Furthermore, ferrostatin-1 reduced iron and ROS deposition to alleviate ferroptosis, thereafter reducing WMI to promote the recovery of motor function. The nuclear factor erythroid-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway was found to be involved in alleviating ferroptosis as seen with the administration of ferrostatin-1. The present study rationalizes that targeting ferroptosis to alleviate WMI is a feasible therapeutic strategy for managing ACMP.

引用

页码：1157 / 1174

页数：18

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