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The three hallmarks of ferroptosis intersect with the pathogenesis of BD, including iron dysregulation, lipid peroxidation, and the failure of antioxidant systems

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While iron is stored safely in ferritin in the injured spinal cord, it can, however, be released by NCOA4-mediated shuttling of ferritin to autophagosomes for degradation (ferritinophagy)

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