ArticleInflammation2023
TNFα-Induced Altered miRNA Expression Links to NF-κB Signaling Pathway in Endometriosis.
Article in Inflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 2 of them syntheses that pooled it.
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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
19 citing papers in PubMed, 2 syntheses or guidelines pooled it, 20 citations in OpenAlex.
- Diagnostic value of MiRNAs in endometriosis: a systematic review and meta-analysis.BMC women's health · 2026Pooled it
- Proteomics approach to discovering non-invasive diagnostic biomarkers and understanding the pathogenesis of endometriosis: a systematic review and meta-analysis.Journal of translational medicine · 2024Pooled it
- Phytochemicals Modulating Receptor Tyrosine Kinase Signaling Networks in Endometriosis.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Endothelial cell heterogeneity drives angiogenesis in endometriosis: mechanisms and emerging organoid-based models.Apoptosis : an international journal on programmed cell death · 2026Review
- Multi-Target Modulation of Interconnected Pathogenetic Pathways by Natural Bioactive Compounds in Endometriosis.Antioxidants (Basel, Switzerland) · 2026Review
- NLRP1 promotes pyroptosis in endometriosis through the NF-κB signaling pathway.Scientific reports · 2026Article
- The role of tumor necrosis factor alpha in regulating CYFRA 21-1 as a potential biomarker for endometriosis: A cross-sectional study.International journal of reproductive biomedicine · 2026Article
- Polyphenol-Rich Wild Fruits of the Indian Himalayas as a Potential Nutraceutical Candidate for the Management of Endometriosis: A Review.Foods (Basel, Switzerland) · 2026Review
- The Role of Nutrition on the Pathogenesis of Endometriosis.Nutrients · 2026Review
- Review
- Modulation of Nuclear Factor Kappa B Signaling and microRNA Profiles by Adalimumab in LPS-Stimulated Keratinocytes.International journal of molecular sciences · 2025Article
- Balancing Decidualization, Autophagy, and Cellular Senescence for Reproductive Success in Endometriosis Biology.International journal of molecular sciences · 2025Review
- Analysis of the Expression Patterns of Tumor Necrosis Factor Alpha Signaling Pathways and Regulatory MicroRNAs in Astrocytic Tumors.International journal of molecular sciences · 2025Article
- Association between the C-reactive protein-triglyceride-glucose index and endometriosis: a cross-sectional study using data from the national health and nutrition examination survey, 1996-2006.BMC women's health · 2025Article
- α7-Nicotinic Acetylcholine Receptor Activation Modulates BV2 Microglial Plasticity via miR-21/TNF-α/NFκB in Oxygen-Glucose Deprivation/Reoxygenation.Journal of molecular neuroscience : MN · 2024Article
- Oxidative Imbalance in Endometriosis-Related Infertility-The Therapeutic Role of Antioxidants.International journal of molecular sciences · 2024Review
- Association between endometriosis and arthritis: results from NHANES 1999-2006, genetic correlation analysis, and Mendelian randomization study.Frontiers in immunology · 2024Article
- MicroRNAs in Endometriosis: Insights into Inflammation and Progesterone Resistance.International journal of molecular sciences · 2023Review
- Combined targeting of TCF7L1/2, PTEN, CDK6, and BCCIP by microRNA miR-29c-3p is associated with reduced invasion and proliferation of endometriotic cells.Reproductive medicine and biologyArticle
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endometriosis is a common gynecological inflammatory disorder characterized by immune system dysregulation, which is involved in lesion initiation and progression. Studies have demonstrated that several cytokines are associated with the evolution of endometriosis, including tumor necrosis factor-α (TNFα). TNFα is a non-glycosylated cytokine protein with potent inflammatory, cytotoxic, and angiogenic potential. In the current study, we examined the ability of TNFα to induce dysregulation of microRNAs (miRNAs) linked to NFkB signaling pathways, thus contributing to the pathogenesis of endometriosis. Using RT-qPCR, the expression of several miRNAs was quantified in primary cells derived from eutopic endometrium of endometriosis subjects (EESC) and normal endometrial stromal cells (NESC), and also TNFα-treated NESCs. The phosphorylation of the pro-inflammatory molecule NF-κB and the candidates of the survival pathways PI3K, AKT, and ERK was measured by western blot analysis. The elevated secretion of TNFα in EESCs downregulates the expression level of several miRNAs significantly in EESCs compared to NESCs. Also, treatment of NESCs with exogenous TNFα significantly reduced the expression of miRNAs in a dose-dependent manner to levels similar to EESCs. In addition, TNFα significantly increased the phosphorylation of the PI3K, AKT, ERK, and NF-κB signaling pathways. Notably, treatment with curcumin (CUR, diferuloylmethane), an anti-inflammatory polyphenol, significantly increased the expression of dysregulated miRNAs in EESC in a dose-dependent manner. Our findings demonstrate that TNFα is upregulated in EESCs, which subsequently dysregulates the expression of miRNAs, contributing to the pathophysiology of endometriotic cells. CUR effectively inhibits the expression of TNFα, subsequently altering miRNA levels and suppressing the phosphorylation of AKT, ERK, and NF-κB.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.