Recent progress of the role of ferroptosis in the pathogenesis of early brain injury after subarachnoid hemorrhage

Subarachnoid hemorrhage (SAH) leads to ferroptosis with clinical evidence like iron metabolism deregulation, increased lipid peroxitation(LPO) and the inhibition of glutathione/glutathione peroxides 4(GSH/GPX4). Ferroptosis mediated early brain injury (EBI) may occur in the 72-hour period following SAH (EBI-SAH) leads to the poor prognosis of SAH. Pharmacological targeting at ferroptosis mitigate EBI-SAH, provides a new target for future treatment and prevention of EBI-SAH through targeting at ferroptosis.