Research advances in endometriosis-related signaling pathways: A review

review OA: gold CC0 ⤵ 66 in-corpus citations
AI-generated summary by claude@2026-06, 2026-06-07

This review comprehensively analyzes multiple signaling pathways involved in endometriosis development, highlighting their overlap with cancer pathways as potential targets for novel therapeutics.

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Abstract

Endometriosis (EM) is characterized by the existence of endometrial mucosa outside the uterine cavity, which causesinfertility, persistent aches, and a decline in women's quality of life. Both hormone therapies and nonhormone therapies, such as NSAIDs, are ineffective, generic categories of EM drugs. Endometriosis is a benign gynecological condition, yet it shares a number of features with cancer cells, including immune evasion, survival, adhesion, invasion, and angiogenesis. Several endometriosis-related signaling pathways are comprehensively reviewed in this article, including E2, NF-κB, MAPK, ERK, PI3K/Akt/mTOR, YAP, Wnt/β-catenin, Rho/ROCK, TGF-β, VEGF, NO, iron, cytokines and chemokines. To find and develop novel medications for the treatment of EM, it is essential to implicitly determine the molecular pathways that are disordered during EM development. Additionally, research on the shared pathways between EM and tumors can provide hypotheses or suggestions for endometriosis therapeutic targets.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometrium Endometrium Endometrium Endometrium Endometrium Endometrium Endometrium

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.

References (100)

Cited by (50)

Source provenance

europepmc
last seen: 2026-06-11T06:19:48.454388+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-06-04T00:33:50.911596+00:00
License: CC0 · commercial use OK