TY  - JOUR
PY  - 2023//
TI  - Targeting ferroptosis promotes functional recovery by mitigating white matter injury following acute carbon monoxide poisoning
JO  - Molecular neurobiology
A1  - Wang, Shuhong
A1  - Xiong, Binyuan
A1  - Tian, Yin
A1  - Hu, Quan
A1  - Jiang, Xuheng
A1  - Zhang, Ji
A1  - Chen, Lin
A1  - Wang, Ruilie
A1  - Li, Mo
A1  - Zhou, Xin
A1  - Zhang, Tianxi
A1  - Ge, Hongfei
A1  - Yu, Anyong
SP  - ePub
EP  - ePub
VL  - ePub
IS  - ePub
N2  - 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>
LA  - en
SN  - 0893-7648
UR  - http://dx.doi.org/10.1007/s12035-023-03603-5
ID  - ref1
ER  -