Molecular Neurobiology · 12 authors, 4 centres
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In a mouse model of traumatic brain injury, moderate-intensity treadmill exercise reduced ferroptosis markers, neurodegeneration, and cognitive impairments at the chronic stage (44 days post-TBI), and these effects were mediated at least in part via suppression of the STING pathway.
This preclinical study used a mouse model of traumatic brain injury (TBI) to investigate whether moderate-intensity treadmill exercise inhibits ferroptosis via the STING pathway. Male mice underwent TBI or sham surgery, with exercise initiation at 3 days post-injury. At 44 days post-TBI, ferroptosis-related characteristics including abnormal iron homeostasis (elevated Tfr1, decreased Fpn, elevated serum Fe²⁺), decreased glutathione peroxidase 4 (Gpx4), and increased lipid peroxidation were detected in the injured cortex. Treadmill exercise reversed these ferroptosis markers, reduced neurodegeneration, decreased anxiety, and improved spatial memory and social novelty. STING knockdown mimicked exercise effects, while STING overexpression reversed them. Findings suggest exercise may combat chronic ferroptosis post-TBI partly through STING pathway suppression.
