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

González-Ramos R, Reinaldo González-Ramos, Defrère S, Sylvie Defrère, Devoto L, Luigi Devoto
Fertility and sterility · 2012 · doi:10.1016/j.fertnstert.2012.06.021 · PMID:22771029
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Nuclear factor-kappaB dysregulation in endometriosis contributes to inflammation, cell proliferation, and reduced apoptosis, potentially driven by iron overload and oxidative stress.

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This review updates and analyzes published evidence on nuclear factor-kappaB (NF-κB) involvement in endometriosis pathophysiology, synthesizing findings from human tissue and in vivo/in vitro studies. It reports that NF-κB (specifically p65 DNA binding) is physiologically activated in the human endometrium with a cyclic pattern in healthy women, but that this cyclic pattern is altered in patients with endometriosis. The review also finds NF-κB basally activated in peritoneal endometriotic lesions, with higher p65 activity in red compared with black lesions, and describes that NF-κB activity is associated with up-regulation of inflammation and cell proliferation and down-regulation of apoptosis, including via macrophage activation in the context of iron overload and oxidative stress. This paper is centrally about endometriosis — it summarizes NF-κB as a regulator of inflammation and cell survival in endometriosis pathophysiology.

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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.
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Nuclear factor-kappaB: A main regulator of inflammation and cell survival in endometriosis pathophysiology Artículo Open/ Download Publication date 2012Metadata Show full item record Cómo citar González-Ramos, Reinaldo Cómo citar Nuclear factor-kappaB: A main regulator of inflammation and cell survival in endometriosis pathophysiology 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): Nucl Indexation Artículo de publicación SCOPUS Identifier URI: https://repositorio.uchile.cl/handle/2250/165679 DOI: 10.1016/j.fertnstert.2012.06.021 ISSN: 00150282 15565653 Quote Item Fertility and Sterility, Volumen 98, Issue 3, 2018, Pages 520-528 Collections

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Inflammation NF-kappa B Animals Apoptosis Cell Proliferation Cell Survival Endometriosis Endometriosis Female Humans Inflammation Iron Iron NF-kappa B

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