AI Article Synopsis
- The study investigates the link between NR4A1 and fibrotic processes in endometriosis, a condition characterized by excessive fibrosis leading to pain and infertility.
- Researchers found that levels of phosphorylated NR4A1 were higher in endometriotic tissue compared to normal tissue, and TGF-β1 stimulation increased its phosphorylation and fibrotic markers.
- The findings suggest that targeting NR4A1 could provide a therapeutic approach for managing fibrosis in endometriosis, as an NR4A1 agonist reduced fibrotic markers and fibrogenesis in experimental models.
Article Abstract
Background/aims: Excess fibrosis may lead to chronic pain, scarring, and infertility as endometriosis develops and progresses. The pathogenesis of endometriosis has been linked to transforming growth factor-β (TGF-β), the most potent promoter of fibrosis.
Methods: Levels of NR4A1 and P-NR4A1 protein in human endometrial and endometriotic tissue were assessed by western blotting and immunohistochemistry. The expression levels of fibrotic markers in stromal cells were evaluated by real-time PCR. The degree of fibrosis in mouse endometriotic lesions was detected by Masson trichrome and Sirius red staining.
Results: The level of phosphorylated-NR4A1 was higher in ovarian endometriotic tissue than in normal endometrium, and long-term TGF-β1 stimulation phosphorylated NR4A1 in an AKT-dependent manner and then promoted the expression of fibrotic markers. Furthermore, inhibition of NR4A1 in stromal cells increased the TGF-β1-dependent elevated expression of fibrotic markers, and loss of NR4A1 stimulated fibrogenesis in mice with endometriosis. Additionally, Cytosporone B (Csn-B), an NR4A1 agonist, effectively decreased the TGF-β1-dependent elevated expression of fibrotic markers in vitro and significantly inhibited fibrogenesis in vivo.
Conclusion: NR4A1 can regulate fibrosis in endometriosis and may serve as a new target for the treatment of endometriosis.
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| http://dx.doi.org/10.1159/000488838 | DOI Listing |
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