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Two principal mechanisms have been proposed: the classical transferrin-dependent pathway and the transcytosis model ( + is reduced to Fe² + , exported into the cytosol by divalent metal transporter 1 (DMT1), and subsequently released across the abluminal membrane via ferroportin 1 (FPN1), followed by re-oxidation through ceruloplasmin before entering the brain parenchyma (172, 173)
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