Insights into iron and nuclear factor-kappa B (NF-kappaB) involvement in chronic inflammatory processes in peritoneal endometriosis.

Sylvie Defrère, Reinaldo González-Ramos, Jean-Christophe Lousse, Jean‐Christophe Lousse, Sébastien Colette, Olivier Donnez, Jacques Donnez, Anne Van Langendonckt
Histology and histopathology · 2011 · vol. 26(8) , pp. 1083–92 · doi:10.14670/hh-26.1083 · PMID:21692040 · W1508912333
review OA: green CC0 ⤵ 47 in-corpus citations
🔓 Open OA copy Full text JSON View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This review examines the roles of excess iron and activated NF-kappaB signaling in the chronic inflammation underlying peritoneal endometriosis, highlighting their potential link and involvement in disease development.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

⚙ AI-generated deep summary by claude@2026-06, 2026-06-09 · read from full text ⓘ

This 2011 review examines how iron overload and the redox-sensitive transcription factor NF-κB are implicated in chronic inflammatory processes in peritoneal endometriosis. It synthesizes prior evidence from endometriosis patients showing increased iron across peritoneal fluid, endometriotic lesions, peritoneum, and macrophages, and explains that excess iron can promote reactive oxygen species that alter gene expression through NF-κB. The review further reports that NF-κB is activated in endometriotic lesions and peritoneal macrophages, leading to increased proinflammatory cytokine production and a positive feedback loop that supports lesion establishment, maintenance, and development, while noting that the work is a narrative review rather than new experimental data. This paper is centrally about endometriosis — it specifically focuses on the involvement of iron and NF-κB in peritoneal endometriosis inflammatory mechanisms.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

Abstract

Endometriosis is a chronic pelvic inflammatory process. Local inflammation is known to play a role in pain and infertility associated with the disease, and may be extensively involved in molecular and cellular processes leading to endometriosis development. In this review, we focus on two inflammatory mediators clearly implicated in the pathogenesis of endometriosis, iron and NF-kappaB, and their potential association. Iron is essential for all living organisms, but excess iron results in toxicity and is linked to pathological disorders. In endometriosis patients, iron overload has been demonstrated in the different compartments of the peritoneal cavity (peritoneal fluid, endometriotic lesions, peritoneum and macrophages). This iron overload affects numerous mechanisms involved in endometriosis development. Moreover, iron can generate free radical species able to react with a wide range of cellular constituents, inducing cellular damage. Overproduction of reactive oxygen species also impairs cellular function by altering gene expression via regulation of redox-sensitive transcription factors such as NF-kappaB, which is clearly implicated in endometriosis. Indeed, NF-kappaB is activated in endometriotic lesions and peritoneal macrophages of endometriosis patients, which stimulates synthesis of proinflammatory cytokines, generating a positive feedback loop in the NF-kappaB pathway. NF-kappaB-mediated gene transcription promotes a variety of processes, including endometriotic lesion establishment, maintenance and development. In conclusion, iron and NF-kappaB appear to be linked and both are clearly involved in endometriosis development, making these pathways an attractive target for future treatment and prevention of this disease.
Full text 2,684 characters · extracted from oa-doi-fallback · click to expand
Insights into iron and nuclear factor-kappa B (NF-κB) involvement in chronic inflammatory processes in peritoneal endometriosis Sylvie Defrère1, Reinaldo González-Ramos2, Jean-Christophe Lousse1, Sébastien Colette1, Olivier Donnez1, Jacques Donnez1 and Anne Van Langendonckt1 1Université Catholique de Louvain, Institute of Experimental and Clinical Research, Department of Gynecology, Brussels, Belgium and 2Institute of Maternal and Child Research, Obstetrics and Gynecology Department, San Borja-Arriaran Clinical Hospital, School of Medicine, University of Chile, Santiago, Chile. Offprint requests to: Professor Jacques Donnez, Department of Gynecology, Université catholique de Louvain, Cliniques Universitaires St Luc, Avenue Hippocrate 10, 1200 Brussels, Belgium. e-mail: [email protected] Summary. Endometriosis is a chronic pelvic inflammatory process. Local inflammation is known to play a role in pain and infertility associated with the disease, and may be extensively involved in molecular and cellular processes leading to endometriosis development. In this review, we focus on two inflammatory mediators clearly implicated in the pathogenesis of endometriosis, iron and NF-κB, and their potential association. Iron is essential for all living organisms, but excess iron results in toxicity and is linked to pathological disorders. In endometriosis patients, iron overload has been demonstrated in the different compartments of the peritoneal cavity (peritoneal fluid, endometriotic lesions, peritoneum and macrophages). This iron overload affects numerous mechanisms involved in endometriosis development. Moreover, iron can generate free radical species able to react with a wide range of cellular constituents, inducing cellular damage. Overproduction of reactive oxygen species also impairs cellular function by altering gene expression via regulation of redox-sensitive transcription factors such as NF-κB, which is clearly implicated in endometriosis. Indeed, NF-κB is activated in endometriotic lesions and peritoneal macrophages of endometriosis patients, which stimulates synthesis of proinflammatory cytokines, generating a positive feedback loop in the NF-κB pathway. NF-κB-mediated gene transcription promotes a variety of processes, including endometriotic lesion establishment, maintenance and development. In conclusion, iron and NF-κB appear to be linked and both are clearly involved in endometriosis development, making these pathways an attractive target for future treatment and prevention of this disease. Histol Histopathol 26, 1083-1092 (2011) Key words: Endometriosis, Inflammation, Iron, NF-kappaB, Macrophage DOI: 10.14670/HH-26.1083

Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.

My notes (saved in your browser only)

⚙ Ask this paper AI returns verbatim quotes from the full text · source: oa-doi-fallback ⓘ

Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works

Condition tags

mesh:D004715endometriosisinfertility

MeSH descriptors

Endometriosis Inflammation Iron Compounds NF-kappa B Peritoneal Diseases Chronic Disease Endometriosis Endometriosis Endometriosis Female Humans Inflammation Inflammation Iron Compounds Iron Overload Iron Overload Iron Overload Iron Overload NF-kappa B Peritoneal Diseases

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.

Cited by (47)

Source provenance

europepmc
last seen: 2026-06-04T01:30:01.192114+00:00
openalex
last seen: 2026-06-04T00:00:01.174412+00:00
pubmed
last seen: 2026-05-13T22:16:42.478857+00:00
License: CC0 · commercial use OK