ArticleEndocrinology2012
Role of estrogen receptor signaling required for endometriosis-like lesion establishment in a mouse model.
Article in Endocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
89 citing papers in PubMed, 2 syntheses or guidelines pooled it, 148 citations in OpenAlex.
- WERF Endometriosis Phenome and Biobanking Harmonisation Project for Experimental Models in Endometriosis Research (EPHect-EM-Homologous): homologous rodent models.Molecular human reproduction · 2025Pooled it
- Diminished Ovarian Reserve in Endometriosis: Insights from In Vitro, In Vivo, and Human Studies-A Systematic Review.International journal of molecular sciences · 2023Pooled it
- YTHDF3 promotes angiogenesis in endometriosis by enhancing the translation efficiency of PFKFB3.Angiogenesis · 2026Article
- Single-Cell RNA Sequencing Shows Markedly Elevated Immune Cell Proportions in the Endometrium of Women with Endometriosis-A Narrative Review.International journal of molecular sciences · 2026Review
- Gut microbial signatures and stability are associated with a co-diagnosis of endometriosis and inflammatory bowel disease.iScience · 2026Article
- Investigation of endothelin-1 receptor antagonist bosentan in a rat endometriosis model.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Establishment of a xenograft model of endometriosis-associated fibrosis using human immortalized endometrial stromal cells overexpressing HOXC8.Scientific reports · 2026Article
- From Inflammation to Malignancy: The Link Between Endometriosis and Gynecological Cancers.International journal of molecular sciences · 2025Review
- Microbiota insights in endometriosis.Microbiome · 2025Review
- From Mice to Primates: Assessing Hormone-Based Endometriosis Models for Preclinical and Therapeutic Insights.Iranian journal of medical sciences · 2025Review
- ESR1 Regulates Fecundity and Functions in Sheep Endometrial Stromal Cells.International journal of molecular sciences · 2025Article
- Targeting steroid receptor coactivators for the treatment of benign female reproductive disorders.Endocrine connections · 2025Review
- Rethinking the Estrogen Receptor Beta Dominance Hypothesis in Endometriosis: Insights from Single Cell RNA Sequencing Meta-analysis.bioRxiv : the preprint server for biology · 2025Article
- Understanding Endometriosis: A Broad Review of Its Causes, Management, and Impact.International journal of molecular sciences · 2025Review
- C57BL/6J mice best recapitulate fibrosis and inflammatory pathophysiology in syngeneic mouse model of endometriosis.Scientific reports · 2025Article
- Gut Microbiota-Derived Acetate Ameliorates Endometriosis via JAK1/STAT3-Mediated M1 Macrophage Polarisation.Microbial biotechnology · 2025Article
- Induction of Endometriosis in a Menstruating Mouse Model (Mus musculus): A Translational Animal Disease Model.Journal of the American Association for Laboratory Animal Science : JAALAS · 2025Article
- The Multifactorial Pathogenesis of Endometriosis: A Narrative Review Integrating Hormonal, Immune, and Microbiome Aspects.Medicina (Kaunas, Lithuania) · 2025Review
- Neutrophils initiate proinflammatory immune responses in early endometriosis lesion development.JCI insight · 2025Article
- RNA sequencing reveals molecular mechanisms of endometriosis lesion development in mice.Disease models & mechanisms · 2024Article
29 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Endometriosis results from ectopic invasion of endometrial tissue within the peritoneal cavity. Aberrant levels of the estrogen receptor (ER), ERα and ERβ, and higher incidence of autoimmune disorders are observed in women with endometriosis. An immunocompetent mouse model of endometriosis was used in which minced uterine tissue from a donor was dispersed into the peritoneal cavity of a recipient. Wild-type (WT), ERα-knockout (αERKO), and βERKO mice were donors or recipients to investigate the roles of ERα, ERβ, and estradiol-mediated signaling on endometriosis-like disease. Mice were treated with vehicle or estradiol, and resulting location, number, and size of endometriosis-like lesions were assessed. In comparison with WT lesions in WT hosts, αERKO lesions in WT hosts were smaller and fewer in number. The effect of ER status and estradiol treatment on nuclear receptor status, proliferation, organization, and inflammation within lesions were examined. αERKO lesions in WT hosts did not form distal to the incision site, respond to estradiol, or proliferate but did have increased inflammation. WT lesions in αERKO hosts did respond to estradiol, proliferate, and show decreased inflammation with treatment, but surprisingly, progesterone receptor expression and localization remained unchanged. Only minor differences were observed between WT lesions in βERKO hosts and βERKO lesions in WT hosts, demonstrating the estradiol-mediated signaling responses are predominately through ERα. In sum, these results suggest ER in both endometriosis-like lesions and their environment influence lesion characteristics, and understanding these interactions may play a critical role in elucidating this enigmatic disease.
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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.