Role of Iron in the Pathogenesis of Endometriosis
Iron accumulates in endometriosis through erythrocyte phagocytosis and subsequent heme processing, leading to iron overload that dysregulates gene expression and causes oxidative stress.
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The paper reviews how iron may contribute to endometriosis pathogenesis by accumulating in peritoneal fluid, macrophages, and endometrial lesions after erythrocyte phagocytosis, leading to hemoglobin release and free iron generation via pathways such as haptoglobin binding or hemeoxygenase-1. Free iron is proposed to be taken up by ferritin and transferrin, promoting iron buildup in macrophages or lesions and dysregulating endometriosis-associated gene expression through oxidative stress. The main caveat is that this is a narrative chapter that synthesizes prior evidence rather than presenting new patient or experimental data. This paper is centrally about endometriosis — it focuses specifically on the role of iron in endometriosis development and related oxidative stress mechanisms.
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