Ferroptosis: a critical player and potential therapeutic target in traumatic brain injury and spinal cord injury

Ferroptosis, a new non-necrotizing programmed cell death (PCD), is driven by iron-dependent phospholipid peroxidation. Ferroptosis plays a key role in secondary traumatic brain injury and secondary spinal cord injury and is closely related to inflammation, immunity, and chronic injuries. The inhibitors against ferroptosis effectively improve iron homeostasis, lipid metabolism, redox stabilization, neuronal remodeling, and functional recovery after trauma. In this review, we elaborate on the latest molecular mechanisms of ferroptosis, emphasize its role in secondary central nervous trauma, and update the medicines used to suppress ferroptosis following injuries.

Automated summary

Ferroptosis is a new form of programmed cell death that is not necrotic and is caused by iron-dependent phospholipid peroxidation. It plays a key role in secondary traumatic brain injury and secondary spinal cord injury and is closely related to inflammation, immunity, and chronic injuries. Inhibitors against ferroptosis effectively improve iron homeostasis, lipid metabolism, redox stabilization, neuronal remodeling, and functional recovery after trauma. This review elaborates on the latest molecular mechanisms of ferroptosis, emphasizes its role in secondary central nervous trauma, and updates the medicines used to suppress ferroptosis following injuries.