FGF21 maintains redox homeostasis and promotes neuronal survival after traumatic brain injury by targeting SLC25A39-mediated mitochondrial GSH transport

Our findings provide preliminary evidence that FGF21 confers protective effects against mitochondrial oxidative stress-related damage following TBI. Additionally, we elucidated a novel role for SLC25A39-dependent mitochondrial GSH transport in both the pathological processes subsequent to TBI and the physiological functions of FGF21.