The DOI matches its Crossref record; 62 of the 73 references it cites were found in a registry or an index; none of the 18 sources its claims cite is checked for support yet.
Role of Estrogen Receptor-β in Endometriosis
Open accessAbstract
Endometriosis is an estrogen-dependent disease. The biologically active estrogen, estradiol, aggravates the pathological processes (e.g., inflammation and growth) and the symptoms (e.g., pain) associated with endometriosis. Abundant quantities of estradiol are available for endometriotic tissue via several mechanisms including local aromatase expression. The question remains, then, what mediates estradiol action. Because estrogen receptor (ER)β levels in endometriosis are >100 times higher than those in endometrial tissue, this review focuses on this nuclear receptor. Deficient methylation of the ERβ promoter results in pathological overexpression of ERβ in endometriotic stromal cells. High levels of ERβ suppress ERα expression. A severely high ERβ-to-ERα ratio in endometriotic stromal cells is associated with suppressed progesterone receptor and increased cyclo-oxygenase-2 levels contributing to progesterone resistance and inflammation. ERβ-selective estradiol antagonists may serve as novel therapeutics of endometriosis in the future.
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21 Own interpretation · 18 Own result · 14 Sources not found · 3 No basis given · 1 Own method
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“We identified a CpG island occupying the promoter region of the ERβ gene (Fig. 3).”
§ Role of Estrogen Receptor-β in Endometriosis > Epigenetic Regulation of the ERβ Promoter is Responsible for Its High Levels in Endometriosis
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“Among these nuclear receptors, ERβ expression is maybe >100 times higher in endometriotic tissue than in endometrium.”
§ Role of Estrogen Receptor-β in Endometriosis > Summary
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Deficient methylation of the ERβ promoter results in pathological overexpression of ERβ in endometriotic stromal cells.”
- Also stated in: § Epigenetic Regulation of the ERβ Promoter is Responsible for Its High Levels in Endometriosis · boosted
“Thus high ERβ mRNA and protein expression in endometriotic cells were mediated by an epigenetic defect involving hypomethylation of a CpG island occupying its promoter (Fig. 3).”
§ Role of Estrogen Receptor-β in Endometriosis > Abstract
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- Also stated in: § Epigenetic Regulation of the ERβ Promoter is Responsible for Its High Levels in Endometriosis · boosted
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In the paper
“ERα mRNA and protein levels are several fold lower in endometriotic tissue and stromal cells compared with endometrial tissue and stromal cells.”
§ Role of Estrogen Receptor-β in Endometriosis > ERβ Is Responsible for Low ERα Expression in Endometriotic Stromal Cells
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“The activity of the ERβ promoter was strongly inactivated by in vitro methylation.”
§ Role of Estrogen Receptor-β in Endometriosis > Epigenetic Regulation of the ERβ Promoter is Responsible for Its High Levels in Endometriosis
boosteddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“In addition to ERα, ERβ, and PR, the orphan nuclear receptor SF1 is also differentially regulated in endometriosis versus eutopic endometrium (Fig. 2).”
§ Role of Estrogen Receptor-β in Endometriosis > Nuclear Receptor Expression in Endometriosis
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In the paper
“ERβ knockdown or overexpression most drastically altered ERα mRNA species arising from the far distal promoter C.”
§ Role of Estrogen Receptor-β in Endometriosis > ERβ Is Responsible for Low ERα Expression in Endometriotic Stromal Cells
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“In contrast, ERα bound to neither promoter C sequences.”
§ Role of Estrogen Receptor-β in Endometriosis > ERβ Is Responsible for Low ERα Expression in Endometriotic Stromal Cells
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Ovarian endometriotic tissue SF1 and ERβ mRNA levels were >12,000 times and 142 times higher than in endometrium, respectively.”
§ Role of Estrogen Receptor-β in Endometriosis > Nuclear Receptor Expression in Endometriosis
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Treatment with a demethylating agent significantly increased ERβ mRNA levels in endometrial cells.”
§ Role of Estrogen Receptor-β in Endometriosis > Epigenetic Regulation of the ERβ Promoter is Responsible for Its High Levels in Endometriosis
plaindirect- Asserted: passes — The authors put it forward as true.
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- It may state two separate claims as one. 9
- Probably not a substantial claim. 2
- The quote only partly states this claim. 1
In the paper
“ERβ mRNA was strikingly higher (~34-fold) in endometriotic stromal cells, whereas it was much lower or nearly absent in endometrial stromal cells.38”
§ Role of Estrogen Receptor-β in Endometriosis > Primary Endometriotic Stromal Cells Mimic Tissue Levels of ERα, ERβ, and PR mRNA and Protein Levels
What the sources say
- Not matchedcites [38]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“The ratios of ERα to ERβ mRNA levels were, on average, 841 and 21 in endometrial and endometriotic stromal cells, respectively.38”
§ Role of Estrogen Receptor-β in Endometriosis > Primary Endometriotic Stromal Cells Mimic Tissue Levels of ERα, ERβ, and PR mRNA and Protein Levels
What the sources say
- Not matchedcites [38]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“ERβ suppresses ERα expression and results in strikingly high ERβ-to-ERα ratios in endometriotic cells.”
§ Role of Estrogen Receptor-β in Endometriosis > Summary
plaindirect- Asserted: passes — The authors put it forward as true.
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- Based: unclear — It is unclear why the paper says it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Endometriotic stromal cells contained extraordinarily higher ERβ and significantly lower ERα and PR levels compared with endometrial stromal cells.”
§ Role of Estrogen Receptor-β in Endometriosis > Primary Endometriotic Stromal Cells Mimic Tissue Levels of ERα, ERβ, and PR mRNA and Protein Levels
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Protein levels of ERα and ERβ were significantly different in these two groups similar to the findings regarding mRNA levels.38”
§ Role of Estrogen Receptor-β in Endometriosis > Primary Endometriotic Stromal Cells Mimic Tissue Levels of ERα, ERβ, and PR mRNA and Protein Levels
What the sources say
- Not matchedcites [38]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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- Not matched
In the paper
“Abundant quantities of estradiol are available for endometriotic tissue via several mechanisms including local aromatase expression.”
§ Role of Estrogen Receptor-β in Endometriosis > Abstract
What the sources say
- Not matchedcites [26]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This proposed mechanism may explain severely deficient PR-B in endometriotic stromal cells, which contributes to progesterone resistance in women with endometriosis.”
§ Role of Estrogen Receptor-β in Endometriosis > Summary
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“A role of ERα promoter A could not be ruled out.”
§ Role of Estrogen Receptor-β in Endometriosis > ERβ Is Responsible for Low ERα Expression in Endometriotic Stromal Cells
hedgedconditional- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. The quote only partly states this claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Estradiol, which reaches endometriosis by circulation or is produced locally in endometriotic tissue, acts as a steroid hormone to regulate growth of endometriotic tissue.”
§ Role of Estrogen Receptor-β in Endometriosis > Nuclear Receptor Expression in Endometriosis
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Circumstantial and laboratory evidence strongly support the notion that estradiol is a key hormone for the growth and persistence of endometriotic tissue as well as inflammation and pain associated with it.”
§ Role of Estrogen Receptor-β in Endometriosis > Nuclear Receptor Expression in Endometriosis
boostedcorrelational- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“It is likely that ERβ simulates prostaglandin production in endometriotic tissues and cells via inducing COX2 expression.”
§ Role of Estrogen Receptor-β in Endometriosis > Summary
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
The paper relies on this without support.
Progestin or oral contraceptive treatment does not reliably suppress the growth of endometriotic tissue.
“Treatment with these agents, however, does not predictably suppress endometriotic tissue growth.”
The paper relies on this without support.
Prolonged progestin therapy or oral contraceptives containing progestins reliably cause atrophy of eutopic endometrium.
“The eutopic endometrium predictably becomes atrophic in response to prolonged progestin therapy or oral contraceptives that contain progestins.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The cited source doesn’t support the claim as written.
In the citing paper
“ERβ is the predominant isoform in patients with endometriosis [7,8].”
From Polymorphisms in the 3 ′ UTR Region of ESR2 and CYP19A1 Genes and Its Influence on Allele-Specific Gene Expression in Endometriosis (2020) · cites this paper as [7]
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Comparison between the patterns of expression of receptor proteins in normal endometrium with samples of endometrial cancer and endometriosis lesions has revealed evidence of aberrant expression of both AR and ERs, which may result in novel disease-specific targets for the action of steroids generated by intracrine activation/metabolism discussed below.”
From Endometrial Intracrinology: Oestrogens, Androgens and Endometrial Disorders (2018) · cites this paper as [35]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Furthermore, the highly expressed oestrogen in endometriotic tissue is present in its most biologically active form [14,15].”
From HRT in Women Undergoing Pelvic Clearance for Endometriosis—A Case Report and a National Survey (2023) · cites this paper as [15]
The cited source says what the claim attributes to it.
In the citing paper
“Molecular studies have revealed the overexpression of oestrogen receptor beta (ERβ), which is >100 times higher in endometriotic lesions compared to normal endometrial tissue.”
From HRT in Women Undergoing Pelvic Clearance for Endometriosis—A Case Report and a National Survey (2023) · cites this paper as [15]
In the citing paper
“A recently published meta-analysis showed that in addition to the above-mentioned variants, gene variants for interferon γ (IFNG CA repeat) and variants of rs16826658 and rs2235529 of the WNT4 gene may be relevant.”
From Endometriosis: Epidemiology, Classification, Pathogenesis, Treatment and Genetics (Review of Literature) (2021) · cites this paper as [198]
In the citing paper
“The ERβ receptor encoded by the ESR2 gene is the dominant isoform in those with endometriosis [198].”
From Endometriosis: Epidemiology, Classification, Pathogenesis, Treatment and Genetics (Review of Literature) (2021) · cites this paper as [198]
In the citing paper
“An unknown trend was also confirmed for the progesterone receptor (PGR) gene variant, the rs1799969 variants of the ICAM1 molecule, rs2292596 of the aromatic hydrocarbon receptor repressor gene (AHRR), the CYP17A1 rs743572 gene and the rs1801282 gene for the peroxisome γ proliferator-activated receptor (PPARγ–peroxisome proliferator-activated receptor γ) [198].”
From Endometriosis: Epidemiology, Classification, Pathogenesis, Treatment and Genetics (Review of Literature) (2021) · cites this paper as [198]
In the citing paper
“Estrogen receptors, acting as transcription factors, play a significant role in endometrial growth and differentiation, as well as in numerous biological functions in eutopic endometrium and endometriosis.”
From Endometriosis: Epidemiology, Classification, Pathogenesis, Treatment and Genetics (Review of Literature) (2021) · cites this paper as [198]
In the citing paper
“Symptoms occur after puberty and oestrogen action contributes to pathological processes including growth of lesions and inflammation, and to the symptoms including pain4142.”
From Meta-analysis identifies five novel loci associated with endometriosis highlighting key genes involved in hormone metabolism (2017) · cites this paper as [41]
In the citing paper
“Endometriosis is an oestrogen-dependent disease.”
From Meta-analysis identifies five novel loci associated with endometriosis highlighting key genes involved in hormone metabolism (2017) · cites this paper as [41]
In the citing paper
“Expression of estrogen receptor b (ER-b) is significantly higher in endometriosis due to the hypermethylation of the CpG islands in the estrogen receptor 2 gene.25,26”
From Altered genome-wide methylation in endometriosis (2014) · cites this paper as [25]
Citations
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“46 49 Two major transcriptional start sites have been identi fi ed.”
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Metadata
- Authors
- Bulun, S., Monsavais, D., Pavone, M., Dyson, M., Xue, Q., Attar, E., Tokunaga, H., & Su, E.
- Affiliations
- Northwestern University (US)
- Peking University First Hospital (CN)
- Istanbul University-Cerrahpaşa (TR)
- Tohoku University (JP)
- Venue
- Seminars in Reproductive Medicine
- Publisher
- Georg Thieme Verlag KG
- Published
- 2012-01
- Volume
- 30
- Issue
- 01
- Pages
- 39-45
- ISSN
- 1526-4564 (ISSN-L)
- 1526-8004
- PMC
- PMC4034571
- OpenAlex
- W2045579344
- Cited by
- 321
- References
- 73
- Citations by year
- 2026: 25 · 2025: 30 · 2024: 31 · 2023: 25 · 2022: 35 · 2021: 24 · 2020: 20 · 2019: 22 · 2018: 22 · 2017: 13 · 2016: 13 · 2015: 23 · 2014: 18 · 2013: 16 · 2012: 4
- FWCI
- 2.67
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Seminars in Reproductive Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Japan Society for the Promotion of Science (23791805)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (R37-HD37691, K12HD050121)
- Topics
- Health Sciences › Medicine › Reproductive Medicine › Endometriosis Research and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Estrogen and related hormone effects
- Health Sciences › Medicine › Obstetrics and Gynecology › Endometrial and Cervical Cancer Treatments
- Keywords
- endometriosis, estrogen receptor beta, estradiol, aromatase, endometriotic stromal cells, promoter methylation, estrogen receptor alpha, progesterone resistance, cyclooxygenase-2, inflammation, nuclear receptors
- MeSH terms
- Animals, Endometriosis, Endometrium, Estrogen Antagonists, Estrogens, Female, Gene Expression Regulation, Humans, Promoter Regions, Genetic, Receptors, Progesterone, Signal Transduction, Stromal Cells, Epigenesis, Genetic, Estrogen Receptor alpha, Estrogen Receptor beta, Cyclooxygenase 2, Steroidogenic Factor 1, Molecular Targeted Therapy
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