ArticleCell2015
Estrogen Receptor β Modulates Apoptosis Complexes and the Inflammasome to Drive the Pathogenesis of Endometriosis.
Article in Cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 214 papers, 2 of them syntheses that pooled it.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
214 citing papers in PubMed, 2 syntheses or guidelines pooled it, 363 citations in OpenAlex.
- An Overview of Essential Nutritional Strategies and Products in the Treatment of Endometriosis.Nutrients · 2025Pooled it
- Pharmaceuticals targeting signaling pathways of endometriosis as potential new medical treatment: A review.Medicinal research reviews · 2021Pooled it
- Elinzanetant (NT-814), a Neurokinin 1,3 Receptor Antagonist, Reduces Estradiol and Progesterone in Healthy Women.The Journal of clinical endocrinology and metabolism · 2021Trial
- Establishment of pathology-validated immortalized patient-derived ovarian endometriosis epithelial cell line.Biomedical reports · 2026Article
- YTHDF3 promotes angiogenesis in endometriosis by enhancing the translation efficiency of PFKFB3.Angiogenesis · 2026Article
- Supraphysiological Estrogen Induces Endometrial Impairments via Mitochondrial ROS-Driven NLRP3 Inflammasome Activation.Antioxidants (Basel, Switzerland) · 2026Article
- Oocyte quality in endometriosis-associated infertility: a narrative analysis of mechanisms and therapeutic options.Molecular biology reports · 2026Review
- Recent insights in pathogenesis of endometriosis with focus on gut microbiota.Molecular biology reports · 2026Review
- Comprehensive transcript and protein profiling reveals ERα rather than ERβ as the predominant estrogen receptor in human endometriotic lesions.Communications biology · 2026Article
- RNF34 restrains endometriosis through SREBP1-dependent metabolic-immune crosstalk.Cellular and molecular life sciences : CMLS · 2026Article
- Emerging signal transduction pathways and the role of bacterial extracellular vesicles linked to the pathogenesis of endometriosis.Communications medicine · 2026Review
- Transfer RNA-derived small RNAs in female reproductive disorders: emerging roles and clinical implications.Journal of assisted reproduction and genetics · 2026Review
- The Microbiota-Endometriosis Axis: An Immune-Endocrine Integration Model and Emerging Therapeutic Targets.International journal of molecular sciences · 2026Review
- Hormonal Dysregulation and Neuroinflammation in Endometriosis: Convergent Druggable Pathways.Current issues in molecular biology · 2026Review
- Nuclear factor IX promotes endometriosis progression through transcriptional activation of tetraspanin-2.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Contributions of T-helper 9 cells in endometriosis-associated inflammation and lesion growth.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Mechanistic insights into inflammatory cytokines in adenomyosis‑induced infertility (Review).International journal of molecular medicine · 2026Review
- Eutopic echoes ectopic: organoid-based evidence of shared hormone dysregulation in endometriosis.Reproductive biology and endocrinology : RB&E · 2026Article
- Pathogenesis of Adenomyosis: An Integrated Review of Cellular Origins, Molecular Mechanisms, and Intersecting Diseases.Journal of cellular and molecular medicine · 2026Review
- Misregulated alternative splicing in endometriosis: a role for aberrant mRNA variants in endometriotic cell growth.Cell death discovery · 2026Article
154 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
Alterations in estrogen-mediated cellular signaling play an essential role in the pathogenesis of endometriosis. In addition to higher estrogen receptor (ER) β levels, enhanced ERβ activity was detected in endometriotic tissues, and the inhibition of enhanced ERβ activity by an ERβ-selective antagonist suppressed mouse ectopic lesion growth. Notably, gain of ERβ function stimulated the progression of endometriosis. As a mechanism to evade endogenous immune surveillance for cell survival, ERβ interacts with cellular apoptotic machinery in the cytoplasm to inhibit TNF-α-induced apoptosis. ERβ also interacts with components of the cytoplasmic inflammasome to increase interleukin-1β and thus enhance its cellular adhesion and proliferation properties. Furthermore, this gain of ERβ function enhances epithelial-mesenchymal transition signaling, thereby increasing the invasion activity of endometriotic tissues for establishment of ectopic lesions. Collectively, we reveal how endometrial tissue generated by retrograde menstruation can escape immune surveillance and develop into sustained ectopic lesions via gain of ERβ function.
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What OpenQuestion holds
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.