Targeting Ferroptosis Promotes Functional Recovery by Mitigating White Matter Injury Following Acute Carbon Monoxide Poisoning.
Shuhong WangBinyuan XiongYin TianQuan HuXuheng JiangJi ZhangLin ChenRuilie WangMo LiXin ZhouTianxi ZhangHongfei GeAnyong YuPublished in: Molecular neurobiology (2023)
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.
Keyphrases
- cell death
- white matter
- reactive oxygen species
- nuclear factor
- drug induced
- liver failure
- signaling pathway
- oxidative stress
- diabetic rats
- high glucose
- toll like receptor
- respiratory failure
- multiple sclerosis
- dna damage
- pi k akt
- epithelial mesenchymal transition
- aortic dissection
- cell proliferation
- immune response
- inflammatory response
- endothelial cells
- hepatitis b virus