The role of NF-kappaB in endometriosis

Kaponis A, Apostolos Kaponis, Tasuku Harada, Tomio Iwabe, Iwabe T, Taniguchi F, Fuminori Taniguchi, Ito M, Masayuki Ito, Deura I, Imari Deura, George Decavalas, Naoki Terakawa, Terakawa N, Harada T
Frontiers in bioscience (Scholar edition) · 2012 · vol. S4(4) , pp. 1213–1234 · doi:10.2741/s327 · PMID:22652867 · W2343207388
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This review discusses the critical role of NF-kappaB in endometriosis pathophysiology, detailing its involvement in inflammation, invasion, vascularization, oxidative stress, and its modulation by therapeutic agents.

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⚙ AI-generated deep summary by claude@2026-07, 2026-07-09 · read from full text ⓘ

This paper is a review describing how the nuclear factor kappaB (NF-κB) transcription factor contributes to endometriosis pathophysiology, drawing on evidence that NF-κB is constitutively activated in endometriotic lesions. It discusses mechanistic interactions between NF-κB, steroid receptors, and apoptotic molecules, noting opposing roles, and describes NF-κB–driven regulation of cytokines that can form self-amplifying autocrine inflammatory cycles. The review also covers how NF-κB may promote invasion and adhesion via regulation of matrix metalloproteinases, and it addresses roles in vascularization and oxidative stress, as well as how drugs used for endometriosis affect the NF-κB pathway. The paper does not state a formal limitation typical of primary studies, but it is an integrative review compiling prior findings rather than presenting new experimental data. This paper is centrally about endometriosis — it focuses on NF-kappaB’s roles in inflammation, invasion, vascularization, oxidative stress, and drug effects in endometriotic lesions.

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Abstract

The nuclear factor kappaB (NF-kappaB) is a ubiquitously expressed transcription factor playing vital roles in innate immunity and other processes involving cellular survival, proliferation, and differentiation. This review highlights the importance of NF-kappaB in the pathophysiology of endometriosis. Constitutive activation of NF-kappaB has been shown in endometriotic lesions. Complex interactions of NF-kappaB with steroid receptors and apoptotic molecules in endometriosis resulting in opposing roles of NF-kappaB are discussed. NF-kappaB regulates the expression of cytokines mediating autocrine self-amplifying cycles of cytokine release and NF-kappaB activation, leading to maintenance of inflammatory reactions in endometriosis. NF-kappaB can contribute to the increased ability of endometriotic cells to invade and adhere to the peritoneal surface by regulating the expression of matrix metaloproteinases. We are presenting the role of NF-kappaB to regulate vascularization and oxidative stress in endometriotic cells. Effects of drugs used for the treatment of endometriosis on NF-kappaB pathway are presented and we show how drugs that inhibit the NF-kappaB can mediate the progression of endometriosis. Novel therapeutic strategies involving the NF-kappaB and applied in endometriosis are also discussed.
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Frontiers in Bioscience-Scholar (FBS) is published by IMR Press from Volume 13 Issue 1 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience. 1 Department of Obstetrics and Gynecology, Patra University School of Medicine, Patra, Greece 2 Department of Obstetrics and Gynecology, Tottori University Faculty of Medicine, Yonago, Japan *Author to whom correspondence should be addressed. Abstract The nuclear factor kappaB (NF-kappaB) is a ubiquitously expressed transcription factor playing vital roles in innate immunity and other processes involving cellular survival, proliferation, and differentiation. This review highlights the importance of NF-kappaB in the pathophysiology of endometriosis. Constitutive activation of NF-kappaB has been shown in endometriotic lesions. Complex interactions of NF-kappaB with steroid receptors and apoptotic molecules in endometriosis resulting in opposing roles of NF-kappaB are discussed. NF-kappaB regulates the expression of cytokines mediating autocrine self-amplifying cycles of cytokine release and NF-kappaB activation, leading to maintenance of inflammatory reactions in endometriosis. NF-kappaB can contribute to the increased ability of endometriotic cells to invade and adhere to the peritoneal surface by regulating the expression of matrix metaloproteinases. We are presenting the role of NF-kappaB to regulate vascularization and oxidative stress in endometriotic cells. Effects of drugs used for the treatment of endometriosis on NF-kappaB pathway are presented and we show how drugs that inhibit the NF-kappaB can mediate the progression of endometriosis. Novel therapeutic strategies involving the NF-kappaB and applied in endometriosis are also discussed.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis NF-kappa B Animals Endometriosis Endometriosis Female Humans NF-kappa B Signal Transduction

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

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