Role of iron overload-induced macrophage apoptosis in the pathogenesis of peritoneal endometriosis

Leila Pirdel, Manijeh Pirdel
Reproduction (Cambridge, England) · 2014 · vol. 147(6) , pp. R199–R207 · doi:10.1530/rep-13-0552 · PMID:24599836 · W2141784155
review OA: bronze CC0 ⤵ 36 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-06 ⓘ

This paper examines how iron overload in peritoneal macrophages triggers nitric oxide overproduction and apoptosis, potentially contributing to endometriosis development and impaired endometrial cell clearance.

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Abstract

This article presents an overview of the involvement of iron overload-induced nitric oxide (NO) overproduction in apoptosis of peritoneal macrophages of women with endometriosis. We have postulated that the peritoneal iron overload originated from retrograde menstruation or bleeding lesions in the ectopic endometrium, which may contribute to the development of endometriosis by a wide range of mechanisms, including oxidative damage and chronic inflammation. Excessive NO production may also be associated with impaired clearance of endometrial cells by macrophages, which promotes cell growth in the peritoneal cavity. Therefore, further research of the mechanisms and consequences of macrophage apoptosis in endometriosis helps discover novel therapeutic strategies that are designed to prevent progression of endometriosis.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Apoptosis Endometriosis Endometrium Iron Overload Iron Overload Macrophages Peritoneal Diseases Animals Endometriosis Endometriosis Endometriosis Endometrium Endometrium Female Humans Iron Overload Iron Overload Macrophages Macrophages Nitric Oxide

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (100)

Cited by (36)

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License: CC0 · commercial use OK