Involvement of the nuclear factor-κB pathway in the pathogenesis of endometriosis

González-Ramos R, Reinaldo González-Ramos, Anne Van Langendonckt, Van Langendonckt A, Defrère S, Sylvie Defrère, Lousse JC, Jean-Christophe Lousse, Jean‐Christophe Lousse, Colette S, Sébastien Colette, Sebastien Colette, Devoto L, Luigi Devoto, Jacques Donnez, Donnez J
Fertility and sterility · 2010 · vol. 94(6) , pp. 1985–1994 · doi:10.1016/j.fertnstert.2010.01.013 · PMID:20188363 · W2035214296
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This paper investigates the role of the nuclear factor-κB pathway in the development of endometriosis.

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Abstract

ObjectiveTo evaluate the role of nuclear factor-κB (NF-κB) in the pathogenesis of endometriosis.DesignA literature search was conducted in PubMed to identify all relevant citations.Result(s)Our findings highlight the important role of NF-κB in the pathophysiology of endometriosis. In vitro and in vivo studies show that NF-κB-mediated gene transcription promotes inflammation, invasion, angiogenesis, and cell proliferation and inhibits apoptosis of endometriotic cells. Constitutive activation of NF-κB has been demonstrated in endometriotic lesions and peritoneal macrophages of endometriosis patients. Agents blocking NF-κB are effective inhibitors of endometriosis development and some drugs with known NF-κB inhibitory properties have proved efficient at reducing endometriosis-associated symptoms in women. Iron overload activates NF-κB in macrophages. NF-κB activation in macrophages and ectopic endometrial cells stimulates synthesis of proinflammatory cytokines, generating a positive feedback loop in the NF-κB pathway and promoting endometriotic lesion establishment, maintenance and development.Conclusion(s)NF-κB transcriptional activity modulates key cell processes contributing to the initiation and progression of endometriosis. Because endometriosis is a multifactorial disease, inhibiting NF-κB appears to be a promising strategy for future therapies targeting different cell functions involved in endometriosis development, such as cell adhesion, invasion, angiogenesis, inflammation, proliferation, and apoptosis. Upcoming research will elucidate these hypotheses.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis NF-kappa B Uterine Diseases Animals Endometriosis Endometriosis Endometriosis Endometriosis Female Humans Inflammation Inflammation Models, Biological NF-kappa B NF-kappa B Signal Transduction Signal Transduction Signal Transduction Uterine Diseases Uterine Diseases

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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.

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