Nuclear factor-kappab (NF-kappaB): an unsuspected major culprit in the pathogenesis of endometriosis that is still at large?

Guo SW, Sun-Wei Guo, Sun‐Wei Guo
Gynecologic and obstetric investigation · 2006 · vol. 63(2) , pp. 71–97 · doi:10.1159/000096047 · PMID:17028437 · W2076069868
Review OA: closed CC0 ⤵ 113 in-corpus citations
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This review proposes that the pro-inflammatory transcription factor NF-κB is a major culprit in endometriosis pathogenesis, acting through an autoregulatory loop and targeted by many existing and investigational endometriosis therapies.

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Abstract

Endometriosis, defined as the ectopic presence of endometrial glandular and stromal cells outside the uterine cavity, is a common benign gynecological disorder with an enigmatic pathogenesis. Many genes and gene products have been reported to be altered in endometriosis, yet some of them may not be major culprits but merely unwitting accomplices or even innocent bystanders. Therefore, the identification and apprehension of major culprits in the pathogenesis of endometriosis are crucial to the understanding of the pathogenesis and would help to develop better therapeutics for endometriosis. Although so far NF-kappaB only has left few traces of incriminating fingerprints, several lines of investigation suggest that NF-kappaB, a pivotal pro-inflammatory transcription factor, could promote and maintain endometriosis. Various inflammatory agents, growth factors, and oxidative stress activate NF-kappaB. NF-kappaB proteins themselves and proteins regulated by them have been linked to cellular transformation, proliferation, apoptosis, angiogenesis, and invasion. Interestingly, all existing and nearly all investigational medications for endometriosis appear to act through suppression of NF-kappaB activation. In endometriotic cells, NF-kappaB appears to be constitutively activated, and suppression of NF-kappaB activity by NF-kappaB inhibitors or proteasome inhibitors suppresses proliferation in vitro. Viewing NF-kappaB as a major culprit, an autoregulatory loop model can be postulated, which is consistent with existing data and, more importantly, can explain several puzzling phenomena that are otherwise difficult to interpret based on prevailing theories. This view has immediate and important implications for novel ways to treat endometriosis. Further research is warranted to precisely delineate the roles of NF-kappaB in the pathogenesis of endometriosis and to indict and convict its aiders and abettors.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis NF-kappa B Receptors, Progesterone Endometriosis Endometriosis Endometriosis Endometriosis Endometrium Endometrium Endometrium Female Female Humans Humans NF-kappa B NF-kappa B Receptors, Progesterone Receptors, Progesterone

Citation neighborhood (2-hop)

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. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

References (100)

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