@article{ref1,
title="Targeting ferroptosis promotes functional recovery by mitigating white matter injury following acute carbon monoxide poisoning",
journal="Molecular neurobiology",
year="2023",
author="Wang, Shuhong and Xiong, Binyuan and Tian, Yin and Hu, Quan and Jiang, Xuheng and Zhang, Ji and Chen, Lin and Wang, Ruilie and Li, Mo and Zhou, Xin and Zhang, Tianxi and Ge, Hongfei and Yu, Anyong",
volume="ePub",
number="ePub",
pages="ePub-ePub",
abstract="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.<p /> <p>Language: en</p>",
language="en",
issn="0893-7648",
doi="10.1007/s12035-023-03603-5",
url="http://dx.doi.org/10.1007/s12035-023-03603-5"
}