ArticleJournal of biosciences2017
Estrogen is essential but not sufficient to induce endometriosis.
Article in Journal of biosciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
17 citing papers in PubMed, 33 citations in OpenAlex.
- Estradiol alters actin and protrusion dynamics in endometriotic epithelial cells.Journal of biological physics · 2026Article
- Review
- Graptophyllum pictum (Acanthaceae) relieves some hallmarks of endometriosis in an experimental model in Wistar rats.Reproduction & fertility · 2025Article
- Blood lipids mediate the effects of gut microbiome on endometriosis: a mendelian randomization study.Lipids in health and disease · 2024Article
- Effects of the gut microbiota and its metabolite short-chain fatty acids on endometriosis.Frontiers in cellular and infection microbiology · 2024Review
- Network pharmacology prediction and experimental verification of Rhubarb-Peach Kernel promoting apoptosis in endometriosis.BMC complementary medicine and therapies · 2023Article
- How Do Microorganisms Influence the Development of Endometriosis? Participation of Genital, Intestinal and Oral Microbiota in Metabolic Regulation and Immunopathogenesis of Endometriosis.International journal of molecular sciences · 2023Review
- Endometriosis and dysbiosis: State of art.Frontiers in endocrinology · 2023Review
- Decreased Expression of EZH2 in Granulosa Cells Contributes to Endometriosis-Associated Infertility by Targeting IL-1R2.Endocrinology · 2022Article
- Intricate Connections between the Microbiota and Endometriosis.International journal of molecular sciences · 2021Review
- Integrating Network Pharmacology and Experimental Validation Deciphers the Mechanism of Guizhi Fuling Wan against Adenomyosis.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Involvement of angiotensin II receptor type 1/NF-κB signaling in the development of endometriosis.Experimental and therapeutic medicine · 2020Article
- Spatial and temporal changes in the expression of steroid hormone receptors in mouse model of endometriosis.Journal of assisted reproduction and genetics · 2020Article
- Mouse model for endometriosis is characterized by proliferation and inflammation but not epithelial-to-mesenchymal transition and fibrosis.Journal of biosciences · 2020Article
- Analysis of the relationship between COMT polymorphisms and endometriosis susceptibility.Medicine · 2019Observational
- Villainous role of estrogen in macrophage-nerve interaction in endometriosis.Reproductive biology and endocrinology : RB&E · 2018Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endometriosis is a common gynaecological disorder of unknown aetiology. Among the several factors, estrogen has been implicated as a causative factor in endometriosis. In the present study using mouse model, we assessed the role of estrogen in the initial implantation and growth of endometrium in ectopic locations. Uterine tissues from green fluorescent protein (GFP) mice were transplanted in to the peritoneum of wild type mice in presence and absence of estrogen. As compared to untreated controls, the implantation of uterine tissue at ectopic locations was higher when estrogen was administered to both host and donor animals. However, this effect was not sustained as lesions regressed within 14 days of treatment. Irrespective of the treatment, peritoneal adipose was the most preferred site of lesion establishment. The lesions did not have typical features of the endometriosis (presence of glands and stroma) even after estrogen treatment and the ectopic tissue underwent regression by apoptosis irrespective of treatment. Since estrogen promotes implantation of endometrial tissue to ectopic locations but failure of these ectopic lesions to grow and sustain even in high estrogenic environment we propose that estrogen is necessary but not sufficient to sustain endometriosis.
Indexed as
Identifiers
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.