Citation

Wang S, Xiong B, Tian Y, Hu Q, Jiang X, Zhang J, Chen L, Wang R, Li M, Zhou X, Zhang T, Ge H, Yu A. Mol. Neurobiol. 2023; ePub(ePub): ePub.

Copyright

(Copyright © 2023, Springer)

DOI

10.1007/s12035-023-03603-5

PMID

37697220

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.

Language: en

Keywords

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