Ferroptosis, a regulated form of cell death characterized by iron-dependent lipid peroxidation, has emerged as a key contributor to neuronal damage in various types of brain injury, including traumatic brain injury (TBI) and ischemic brain injury caused by brian ischemia (BI). This review summarizes the underlying mechanisms of ferroptosis in brain injuries and highlights its role in exacerbating neuronal loss, inflammation, and secondary damage. After TBI, the release of free iron and oxidative stress after injury triggers ferroptosis, contributing to long-term neurological deficits. Similarly, in BI, ferroptosis is initiated by the accumulation of reactive oxygen species (ROS) and mitochondrial dysfunction during ischemia and reperfusion, further amplifying neuronal damage. The current review provides a comprehensive overview of the interplay between ferroptosis and brain injury, with an emphasis on the potential of targeting ferroptosis to improve recovery outcomes in patients. Future research directions include the development of novel ferroptosis inhibitors and the integration of ferroptosis-targeting strategies with existing treatment modalities.
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