ArticleJournal of pain research2026
Metabolomics Analysis Reveals Gut Microbiota-Associated Sakuranin Modulates Endometrial Stem Cell Differentiation and Inflammation to Alleviate Pain in Endometriosis.
Article in Journal of pain research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Endometriosis (EMS) is characterized by pain symptoms that seriously affect patients' quality of life. Gut microbiome-related metabolites (GMRM) play an important role in the process of EMS. However, the role of GMRM in endometrial stem cells and EMS-related pain remains unclear. Methods: An untargeted metabolomics approach was employed to analyze the fecal samples of 10 healthy individuals (heal), 11 EMS patients without dysmenorrhea (pless), and 14 EMS patients with dysmenorrhea (pain). The impact of potential key metabolite sakuranin on EMS-related pain was further investigated in vitro and in vivo. Results: We identified 33 metabolites that were commonly changed in the painful group compared to the health and pless groups, and these metabolites were associated with differential microorganisms. Among them, sakuranin was downregulated in the painful group and exhibited a notably inverse correlation with the degree of pain. ROC curve revealed that sakuranin had a relatively high predictive value for EMS-related pain (AUC=0.8027). Functionally, sakuranin inhibited differentiation, migration, and inflammatory cytokine production, and decreased the expression of VEGF and ALCAM in SUSD2-positive primary endometrial cells. In EMS mice, sakuranin suppressed ectopic lesion growth, reduced inflammation, modulated angiogenesis and proliferation markers (VEGF, ALCAM, Ki-67), and regulated sympathetic and sensory nerve markers, resulting in alleviated pain behaviors. Conclusion: We delineated the metabolic landscape related to EMS-related pain and uncovered that sakuranin has the potential to inhibit the growth of EMS and alleviate EMS-related pain. This finding offers therapeutic strategies of sakuranin in alleviating the pain symptoms associated with EMS.
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