Potential involvement of iron in the pathogenesis of peritoneal endometriosis

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This review discusses how iron overload in the pelvic cavity, potentially from retrograde menstruation, may contribute to endometriosis pathogenesis through mechanisms like oxidative stress and lesion proliferation.

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Abstract

The aim of this study is to review the current literature associating endometriosis with iron and to discuss the potential causes and consequences of iron overload in the pelvic cavity. Indeed, iron is essential for all living organisms. However, excess iron can result in toxicity and is associated with pathological disorders. In endometriosis patients, iron overload has been demonstrated in the different components of the peritoneal cavity (peritoneal fluid, endometriotic lesions, peritoneum and macrophages). Animal models allow us to gather essential information on the origin, metabolism and effect of iron overload in endometriosis, which may originate from erythrocytes carried into the pelvic cavity mainly by retrograde menstruation. Peritoneal macrophages play an important role in the degradation of these erythrocytes and in subsequent peritoneal iron metabolism. Iron overload could affect a wide range of mechanisms involved in endometriosis development, such as oxidative stress or lesion proliferation. In conclusion, excess iron accumulation can result in toxicity and may be one of the factors contributing to the development of endometriosis. Treatment with an iron chelator could thus be beneficial in endometriosis patients to prevent iron overload in the pelvic cavity, thereby diminishing its deleterious effect.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Iron Peritoneum Animals Endometriosis Endometriosis Endometriosis Female Humans Iron Iron Iron Overload Iron Overload Iron Overload Models, Biological Oxidative Stress Peritoneum Peritoneum

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europepmc
last seen: 2026-08-21T06:14:13.963979+00:00
pubmed
last seen: 2026-05-13T22:14:30.652814+00:00
unpaywall
last seen: 2026-05-14T19:30:52.867331+00:00
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