Involvement of the Wnt/β-Catenin Signaling Pathway in the Cellular and Molecular Mechanisms of Fibrosis in Endometriosis

Sachiko Matsuzaki, Claude Darcha
PloS one · 2013 · vol. 8(10) , pp. e76808 · doi:10.1371/journal.pone.0076808 · PMID:24124596 · PMC3790725 · W2105973884
article OA: gold CC0 ⤵ 93 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This study investigated the Wnt/β-catenin signaling pathway's role in the cellular and molecular mechanisms underlying fibrosis in endometriotic lesions.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-09 ⓘ

This study examined whether the Wnt/β-catenin signaling pathway regulates fibrotic mechanisms in endometriosis by testing small-molecule antagonists of the Tcf/β-catenin complex (PKF 115-584 and CGP049090) and by activating the pathway with recombinant Wnt3a. Endometrial and endometriotic stromal cells were collected from patients with endometriosis and controls, and the antagonists significantly reduced fibrotic marker expression (αSMA, type I collagen, connective tissue growth factor, and fibronectin) and decreased collagen gel contraction in vitro, including under TGF-β1 stimulation; Wnt3a-driven pathway activation increased profibrotic responses in cells from patients without endometriosis. In a xenograft endometriosis model in immunodeficient nude mice, CGP049090 prevented progression of fibrosis and reversed established fibrosis. The paper’s main limitation is that it assesses fibrosis using selected molecular markers and a xenograft model rather than directly measuring lesion-level clinical outcomes, and it uses cell-based assays and drug exposure in controlled settings. This paper is centrally about endometriosis — specifically, it targets Wnt/β-catenin signaling to modulate fibrosis (fibrogenesis markers and collagen contraction) in endometriotic stromal cells and xenograft implants.

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Abstract

Background: During the development and progression of endometriotic lesions, excess fibrosis may lead to scarring, chronic pain, and altered tissue function. However, the cellular and molecular mechanisms of fibrosis in endometriosis remain to be clarified.

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Condition tags

endometriosis

MeSH descriptors

beta Catenin Endometriosis Endometriosis Wnt Proteins Wnt Signaling Pathway Actins Actins Actins Adult Animals beta Catenin beta Catenin Collagen Collagen Collagen Connective Tissue Growth Factor Connective Tissue Growth Factor Connective Tissue Growth Factor Disease Models, Animal Endometriosis

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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Cited by (50)

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