Document Detail

Involvement of the nuclear factor-κB pathway in the pathogenesis of endometriosis.
MedLine Citation:
PMID:  20188363     Owner:  NLM     Status:  MEDLINE    
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.
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.
Instituto de Investigaciones Materno Infantil, Departamento de Obstetricia y Ginecología, Hospital Clínico San Borja-Arriarán, Facultad de Medicina, Universidad de Chile, Santiago, Chile.
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MeSH Terms
Endometriosis / etiology*,  genetics,  immunology,  metabolism
Inflammation / complications
Models, Biological
NF-kappa B / metabolism,  physiology*
Signal Transduction / genetics,  physiology
Uterine Diseases / etiology*,  genetics,  immunology,  metabolism
Reg. No./Substance:
0/NF-kappa B

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