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This vulnerability is exacerbated by the fine balance between the intracellular iron levels required for maintaining essential cellular functions and the conditions that promote iron overload [12,13]

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Although thyroid hormone production in follicular cells is iron-dependent, iron overloadresulting from hepcidin-mediated ferroportin blockade, macrophage-derived ferritin uptake, and heme catabolismand resultant oxidative stress can trigger their degeneration through the ferroptosis pathway (179)

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