Literature DB >> 22771029

Nuclear factor-kappaB: a main regulator of inflammation and cell survival in endometriosis pathophysiology.

Reinaldo González-Ramos1, Sylvie Defrère, Luigi Devoto.   

Abstract

OBJECTIVE: To update, analyze, and summarize the literature concerning nuclear factor-kappaB (NF-κB) participation in endometriosis pathophysiology.
DESIGN: Review. RESULT(S): Nuclear factor-kappaB is physiologically activated in the human endometrium, showing variable activity. A cyclic p65-DNA binding pattern was shown in the endometrium of healthy women. This cyclic pattern was altered in the endometrium of patients with endometriosis. Nuclear factor-kappaB is basally activated in peritoneal endometriotic lesions, showing higher p65 activity in red endometriotic lesions than in black lesions. In vivo and in vitro studies show up-regulation of inflammation and cell proliferation and down-regulation of apoptosis by NF-κB activity. Iron overload has been shown in the pelvic cavity of endometriosis patients, and iron overload and oxidative stress activate NF-κB in macrophages, which have been shown to participate in the endometriosis-associated inflammatory reaction. CONCLUSION(S): Nuclear factor-kappaB activation dysregulation in the endometrium of endometriosis patients may explain some endometrial biological alterations associated with endometriosis. The scientific evidence strongly suggests that NF-κB activity in endometriotic cells stimulates inflammation and cell proliferation and inhibits apoptosis, favoring the development and maintenance of endometriosis. Iron overload in the pelvic cavity of endometriosis patients could be a main factor enhancing oxidative stress and activating NF-κB in a chronic manner, contributing to endometriosis establishment and growth.
Copyright © 2012 American Society for Reproductive Medicine. Published by Elsevier Inc. All rights reserved.

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Year:  2012        PMID: 22771029     DOI: 10.1016/j.fertnstert.2012.06.021

Source DB:  PubMed          Journal:  Fertil Steril        ISSN: 0015-0282            Impact factor:   7.329


  45 in total

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2.  MiR-182 inhibits proliferation, migration, invasion and inflammation of endometrial stromal cells through deactivation of NF-κB signaling pathway in endometriosis.

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Journal:  Reprod Sci       Date:  2013-05-07       Impact factor: 3.060

Review 4.  The Origin and Pathogenesis of Endometriosis.

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9.  Endometriotic inflammatory microenvironment induced by macrophages can be targeted by niclosamide†.

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10.  Association of the neutrophil-to-lymphocyte ratio and CA 125 with the endometriosis score.

Authors:  Seul Ki Kim; Jung Yeon Park; Byung Chul Jee; Chang Suk Suh; Seok Hyun Kim
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