ArticleScientific reports2026
PARP-1 couples β-catenin/TCF4 signaling to epithelial-mesenchymal transition in endometriosis.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Multi-Target Modulation of Interconnected Pathogenetic Pathways by Natural Bioactive Compounds in Endometriosis.Antioxidants (Basel, Switzerland) · 2026Review
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Authors and funding
7 authors.
Funding
Abstract
Endometriosis exhibits epithelial–mesenchymal transition (EMT)-aligned traits that promote invasion and lesion persistence. We investigated whether poly(ADP-ribose) polymerase-1 (PARP-1) coordinates β-catenin/TCF4 activity with EMT programs and whether these features are amenable to pharmacologic inhibition. PARP-1 and EMT markers were profiled in normal endometrium and ovarian endometriotic lesions. In endometriotic epithelial cells, PARP-1 levels were modulated by overexpression or siRNA and effects on EMT markers and motility were quantified. Association of PARP-1 with β-catenin/TCF4 complexes was evaluated, and a lesion model was used to test the impact of PARP inhibition on EMT features and lesion burden. PARP-1 was elevated in ectopic lesions and aligned with EMT-associated marker shifts. PARP-1 gain increased β-catenin/TCF4 activity, remodeled EMT markers, and enhanced motility, whereas PARP-1 loss produced the opposite pattern. Analyses supported PARP-1 association with β-catenin/TCF4 complexes. Pharmacologic PARP inhibition attenuated β-catenin/TCF4-aligned EMT features in vitro and reduced lesion growth with concurrent marker normalization in vivo. These findings indicate that PARP-1 couples Wnt/β-catenin signaling to EMT programs in endometriosis and identify PARP inhibition as a tractable approach to modulate these phenotypes.
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Registered trials
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