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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)

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]