| Involvement of the nuclear factor-κB pathway in the pathogenesis of endometriosis. | |
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MedLine Citation:
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PMID: 20188363 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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OBJECTIVE: To evaluate the role of nuclear factor-κB (NF-κB) in the pathogenesis of endometriosis. DESIGN: A 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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Authors:
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Reinaldo González-Ramos; Anne Van Langendonckt; Sylvie Defrère; Jean-Christophe Lousse; Sebastien Colette; Luigi Devoto; Jacques Donnez |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Review Date: 2010-02-26 |
Journal Detail:
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Title: Fertility and sterility Volume: 94 ISSN: 1556-5653 ISO Abbreviation: Fertil. Steril. Publication Date: 2010 Nov |
Date Detail:
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Created Date: 2010-10-27 Completed Date: 2010-12-08 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0372772 Medline TA: Fertil Steril Country: United States |
Other Details:
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Languages: eng Pagination: 1985-94 Citation Subset: IM |
Copyright Information:
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Copyright © 2010 American Society for Reproductive Medicine. Published by Elsevier Inc. All rights reserved. |
Affiliation:
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Instituto de Investigaciones Materno Infantil, Departamento de Obstetricia y Ginecología, Hospital Clínico San Borja-Arriarán, Facultad de Medicina, Universidad de Chile, Santiago, Chile. rgonzalezr@med.uchile.cl |
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Endometriosis / etiology*, genetics, immunology, metabolism Female Humans Inflammation / complications Models, Biological NF-kappa B / metabolism, physiology* Signal Transduction / genetics, physiology Uterine Diseases / etiology*, genetics, immunology, metabolism |
| Chemical | |
Reg. No./Substance:
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0/NF-kappa B |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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