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Although compensatory mechanisms such as the prominin2-multivesicular body-exosome-ferritin axis exist, they are insufficient to counteract aberrant iron influx (20), resulting in iron deposition within cells and in gingival connective tissue

reported that unexplained liver injury in PCOS patients and animal models was accompanied by increased Fe deposition and downregulation of hepcidin and GPX4 expression in the liver, indicating the importance of iron metabolism in this type of unexplained liver injury (165)

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