Document Detail


Involvement of the nuclear factor-κB pathway in the pathogenesis of endometriosis.
MedLine Citation:
PMID:  20188363     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Reinaldo González-Ramos; Anne Van Langendonckt; Sylvie Defrère; Jean-Christophe Lousse; Sebastien Colette; Luigi Devoto; Jacques Donnez
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review     Date:  2010-02-26
Journal Detail:
Title:  Fertility and sterility     Volume:  94     ISSN:  1556-5653     ISO Abbreviation:  Fertil. Steril.     Publication Date:  2010 Nov 
Date Detail:
Created Date:  2010-10-27     Completed Date:  2010-12-08     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0372772     Medline TA:  Fertil Steril     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1985-94     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 American Society for Reproductive Medicine. Published by Elsevier Inc. All rights reserved.
Affiliation:
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:
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:
0/NF-kappa B

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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