ArticleScientific reports2020
Dose-dependent pro- or anti-fibrotic responses of endometriotic stromal cells to interleukin-1β and tumor necrosis factor α.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- The role of fibrosis in endometriosis: a systematic review.Human reproduction update · 2024Pooled it
- Exploring the therapeutic potential of cannabidiol in soft tissue wound healing: Delivery strategies and anti-inflammatory pathways.Acta pharmaceutica Sinica. B · 2026Review
- Proposed Role of RGS1 in Modulating IL-1β-IL-1R1-IRAK4-TAK1 Signaling in Endometriotic Stromal Cells.Reproductive sciences (Thousand Oaks, Calif.) · 2026Article
- The P2X7 Receptor Promotes Intestinal Fibrosis by Modulating the Gut Microbiota and the Inflammasome.Cellular and molecular gastroenterology and hepatology · 2026Article
- Unraveling molecular heterogeneity: a systematic review of susceptibility gene profiles in ovarian, deep infiltrating, and superficial peritoneal endometriosis.Frontiers in reproductive health · 2026Review
- Effect of Hydrothermal Coatings of Magnesium AZ31 Alloy on Osteogenic Differentiation of hMSCs: From Gene to Protein Analysis.Materials (Basel, Switzerland) · 2025Article
- Article
- Decreased oocyte quality in patients with endometriosis is closely related to abnormal granulosa cells.Frontiers in endocrinology · 2023Review
- NLRP3 Inflammasome Activation of Mast Cells by EstrogenFrontiers in immunology · 2021Article
- Relaxin-2 May Suppress Endometriosis by Reducing Fibrosis, Scar Formation, and Inflammation.Biomedicines · 2020Article
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endometriosis are characterized by dense fibrous tissue. Numerous studies have investigated roles of inflammation on the pathophysiology of endometriosis. However, the interplay of inflammation and fibrosis remains to be clarified. Here we show that low levels of interleukin-1β (IL-1β) and tumor necrosis factor-alpha (TNFα) promoted a fibrotic phenotype, whereas high levels of IL-1β and TNFα inactivated the fibrotic phenotype of endometriotic stromal cells (Ectopic-ES). IL-1β 10 pg/mL and TNFα 100 and 1,000 pg/mL had minimal effects, whereas the highest dose of IL-1β (100 pg/mL) significantly decreased collagen gel contraction in Ectopic-ES. Furthermore, in Ectopic-ES, low levels of IL-1β (1 pg/mL) and/or TNFα 10 pg/mL significantly increased Col I mRNA expression, whereas higher doses of IL-1β (10 and/or 100 pg/mL) and/or TNFα (100 and/or 1,000 pg/mL) significantly decreased Col I and/or αSMA mRNA expression and the percentage of cells with Col I + and/or αSMA + stress fibers. In contrast, in either menstrual endometrial stromal cells of patients with endometriosis or those of healthy women, varying doses of IL-1β and/or TNFα had no significant effects on either Col I or αSMA mRNA/protein expression. The present findings bring into question whether we should still continue to attempt anti-inflammatory treatment strategies for endometriosis.
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