The interaction between BMAL1, circadian rhythms, and ferroptosis may increase neuronal vulnerability after traumatic brain injury.

TBI may disrupt circadian clocks and promote ferroptosis, a type of cell death.

• Ferroptosis is linked to mechanical and secondary injuries from traumatic brain injury.
• Core circadian clock regulators, BMAL1, CLOCK, and PER2, are disrupted after TBI.
• Iron accumulation and blood-brain barrier leakage accompany neuronal damage in TBI.
• Ferroptosis inhibitors like melatonin and liproxstatin-1 may reduce weight loss and neurological issues post-TBI.
• While both inhibitors affect clock genes, only melatonin restored body temperature rhythms.
• The findings suggest a complex relationship where circadian disruption may worsen ferroptosis.

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