ArticleScientific reports2025
XBP1 promotes endometrial fibrosis through cGAS-STING signaling pathway in intrauterine adhesion.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Integrative subtractive genomics and molecular dynamics-based approach for drug repurposing against female genital tuberculosis.Molecular diversity · 2026Article
- Piezo1 mediates hypoxia-induced endometriosis fibrosis via the mtDNA -dependent cGAS-STING pathway.Journal of translational medicine · 2026Article
- Article
- SB202190 alleviates endometrial fibrosis by modulating the TGF-β/Smad signaling pathway.American journal of translational research · 2026Article
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12 authors.
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Abstract
Intrauterine adhesion (IUA) was characterized by endometrial fibrosis, leading primarily to hypomenorrhea, infertility and recurrent miscarriage. Epithelial-mesenchymal transition (EMT) is now recognized as a key factor in the development of endometrial fibrosis. X-box binding protein 1 (XBP1), as a crucial transcription factor, has emerged as a potential target for anti-fibrosis treatment in the liver due to its role in various tissue fibrosis. However, the function and molecular mechanisms of XBP1 in the endometrium of patients with IUA are not well understood. In this study, we identified abnormal expression of XBP1, epithelial-mesenchymal transition (EMT) markers, and the cGAS-STING pathway in endometrial tissues from patients with IUA and in IUA-like mouse models. XBP1 was found to promote EMT in endometrial epithelial cells by activating the cGAS-STING pathway and cytoplasmic release of mitochondrial DNA. The addition of mitochondrial membrane inhibition VBIT-4 reversed TGF-β1-induced EMT in vitro. Inhibition of XBP1 reduced endometrial fibrosis and the cGAS-STING pathway activity in the IUA-like mouse models, while activation of XBP1 caused the opposite outcome. These findings indicate XBP1 may serve as a potential therapeutic target for IUA.
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