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
plain- Asserted: passes — The authors put it forward as true.
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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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“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
boosteddirect- Asserted: passes — The authors put it forward as true.
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- Also stated in: § Epigenetic Regulation of the ERβ Promoter is Responsible for Its High Levels in Endometriosis · boosted
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
“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 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 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
“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]
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]
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“ERβ is the predominant isoform in patients with endometriosis [7, 8].”
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Imaging of Urinary Bladder and Ureteral Endometriosis with Emphasis on Diagnosis and Technique
Shenoy‐Bhangle, A. S., Franco, I. P., Ray, L. J., Cao, J., Kilcoyne, A., Horvat, N. D. S. M. R., & Chamié, L. P. (2023) · Academic Radiology · doi:10.1016/j.acra.2023.10.053 · Cited by 27
The phenotypic and genetic association between endometriosis and immunological diseases
Shigesi, N., Harris, H. R., Fang, H., Ndungu, A., Lincoln, M. R., Cotsapas, C. J., Knight, J. C., Missmer, S. A., Morris, A. P., Becker, C. M., et al. (2025) · Human Reproduction · doi:10.1093/humrep/deaf062 · Cited by 33
“…is provided both systemically and also from localized production of aromatase (Zondervan et al. , 2020) and expression of oestrogen receptor beta (Bulun et al. , 2012), inhibition of TNF-α -induced apoptosis, increased interleukin-1 β , which enhances cellular adhesion and proliferation, and…”
Zubrzycka, A., Migdalska‐Sęk, M., Jędrzejczyk, S., & Brzeziańska‐Lasota, E. (2021) · Current Issues in Molecular Biology · doi:10.3390/cimb43020064 · Cited by 29
Pedersen, A. L., Brownrout, J., & Saldanha, C. J. (2017) · Physiology & Behavior · doi:10.1016/j.physbeh.2017.10.013 · Cited by 25
“However, although E2 exacerbates inflammation in endometriosis and asthma (Bulun et al., 2012; Keselman and Heller, 2015), the data suggest a strong anti-inflammatory role for this steroid in rheumatoid arthritis and osteoporosis (Sapir-Koren and Livshits, 2017).”
BackgroundAlsbjerg, B., Kesmodel, U. S., & Humaidan, P. (2022) · Reproductive BioMedicine Online · doi:10.1016/j.rbmo.2022.09.005 · Cited by 25
TGF-β Induces Endometriotic Progression via a Noncanonical, KLF11-Mediated Mechanism
Correa, L. F., Zheng, Y., Delaney, A. A., Khan, Z., Shenoy, C. C., & Daftary, G. S. (2016) · Endocrinology · doi:10.1210/en.2016-1194 · Cited by 24
Chang, K., Liu, L.-B., Li, H., Mei, J., Shao, J., Xie, F., Li, M., & Li, D. (2014) · PubMed Central · Cited by 23
Sakhteman, A., Pasdaran, A., Afifi, M., & Hamedi, A. (2020) · Journal of Evidence-Based Integrative Medicine · doi:10.1177/2515690x20932527 · Cited by 22
Smolarz, B., Szyłło, K., & Romanowicz, H. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21218235 · Cited by 23
“In addition, this phenomenon is also affected by deficits of 17β-hydroxysteroid dehydrogenase of type 2 (17β-HSD2), which is responsible for the oxidation of more active estradiol to less active estrone [65].”
BackgroundKobayashi, H., Uekuri, C., & Shigetomi, H. (2013) · Gynecological Endocrinology · doi:10.3109/09513590.2013.831832 · Cited by 21
Le, A., Shan, L., Wang, Z. H., et al. (2015) · Genetics and Molecular Research · doi:10.4238/2015.september.22.19 · Cited by 21
Cozzolino, M., Pellicer, N., Galliano, D., & Pellicer, A. (2022) · Reproductive BioMedicine Online · doi:10.1016/j.rbmo.2022.09.023 · Cited by 24
Estrogen-Induced CCN1 Is Critical for Establishment of Endometriosis-Like Lesions in Mice
Zhao, Y., Li, Q., Katzenellenbogen, B. S., Lau, L. F., Taylor, R. N., Bagchi, I. C., & Bagchi, M. K. (2014) · Molecular Endocrinology · doi:10.1210/me.2014-1080 · Cited by 21
Estrogen restricts the apoptosis of endometrial stromal cells by promoting TSLP secretion
Yang, H.-L., Chang, K.-K., Mei, J., Zhou, W.-J., Liu, L.-B., Yao, L., Meng, Y., Wang, M.-Y., Ha, S., Lai, Z.-Z., et al. (2018) · Molecular Medicine Reports · doi:10.3892/mmr.2018.9428 · Cited by 22
“The expression levels of ER α and ER β of the ectopic endometrial tissues differ to that of eutopic tissues, which possess markedly higher expression levels of ER β (23,24).”
Novel Medicine for Endometriosis and Its Therapeutic Effect in a Mouse Model
Kim, Y., Kim, Y. J., Kim, M., Lee, S. J., Kwon, H., & Lee, J. H. (2020) · Biomedicines · doi:10.3390/biomedicines8120619 · Cited by 21
“The high level of ER-beta in the endometriotic stromal cells may suppress progesterone receptor expression and enhance the cyclo-oxygenase 2 level, which is associated with progesterone resistance and inflammation [45].”
BackgroundLPAR2 and LPAR4 are the Main Receptors Responsible for LPA Actions in Ovarian Endometriotic Cysts
Kowalczyk‐Zieba, I., Wocławek-Potocka, I., Waśniewski, T., Boruszewska, D., Grycmacher, K., Sinderewicz, E., Staszkiewicz‐Chodor, J., & Wołczyński, S. (2018) · Reproductive Sciences · doi:10.1177/1933719118766263 · Cited by 19
García-Gómez, E., Gómez-Viais, Y. I., Cruz-Aranda, M. M., Martínez‐Razo, L. D., Reyes-Mayoral, C., Ibarra-González, L., Montoya-Estrada, A., Osorio‐Caballero, M., Perichart‐Perera, O., Camacho‐Arroyo, I., et al. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24076857 · Cited by 19
The origin of endometriosis-associated ovarian cancer from uterine neoplastic lesions
Garavaglia, E., Sigismondi, C., Ferrari, S. M., & Candiani, M. (2017) · Medical Hypotheses · doi:10.1016/j.mehy.2017.11.006 · Cited by 18
Poor Endometrial Proliferation After Clomiphene is Associated With Altered Estrogen Action
Bressler, L. H., Fritz, M. A., Wu, S., Yuan, L., Kafer, S., Wang, T., DeMayo, F. J., & Young, S. L. (2021) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/clinem/dgab381 · Cited by 18
Innovations in classical hormonal targets for endometriosis
Pluchino, N., Freschi, L., Wenger, J., & Streuli, I. (2015) · Expert Review of Clinical Pharmacology · doi:10.1586/17512433.2016.1129895 · Cited by 19
“Hormonal alterations may influence the ability of endometrial cells to proliferate, attach to the mesothelium, and/or evade immune-mediated clearance.[17] These findings support the capacity of endometriotic”
ResultNew insights on the pathogenesis of endometriosis and novel non-surgical therapies
Suardika, A., & Pemayun, T. G. A. (2018) · Journal of the Turkish-German Gynecological Association · doi:10.4274/jtgga.2018.0090 · Cited by 18
“Prostaglandins are also known to increase the activity of steroidogenic proteins especially aromatase (p450arom) and the production of tissue estrogens, thereby aggravating the condition (22,23).”
BackgroundPPARγ Agonists: Emergent Therapy in Endometriosis
Vallée, A., Vallée, J.-N., Blanche, A. F. L., & Lecarpentier, Y. (2021) · Pharmaceuticals · doi:10.3390/ph14060543 · Cited by 19
“Elevation of COX-2 expression has a main role in the initiation and development of endometriosis [61,62].”
BackgroundBıyık, İ., Kalkan, Ü., & Şimşek, S. (2021) · Taiwanese Journal of Obstetrics and Gynecology · doi:10.1016/j.tjog.2021.09.017 · Cited by 17
Dabi, Y., Suisse, S., Jornéa, L., Bouteiller, D., Touboul, C., Puchar, A., Daraï, É., & Bendifallah, S. (2022) · Diagnostics · doi:10.3390/diagnostics12010175 · Cited by 16
“This latter was reported in the inflammatory process [109].”
BackgroundHamid, F. A., Abu, M., Karim, A. K. A., Ahmad, M., Aziz, N. A., Kamal, D. A. M., & Mokhtar, M. H. (2022) · Biomedicines · doi:10.3390/biomedicines10071705 · Cited by 17
“Oestrogen accumulation occurs in the endometriotic tissues due to the high expression of aromatase and steroidogenic acute regulatory protein, the two enzymes responsible for the conversion of cholesterol into E2 [109].”
BackgroundMouse uterine stem cells are affected by endocrine disruption and initiate uteropathies
Singh, P., & Bhartiya, D. (2022) · Reproduction · doi:10.1530/rep-22-0337 · Cited by 17
Alali, Z., Graham, A. R., Swan, K., Flyckt, R. L., Falcone, T., Cui, W., Yang, X., Christianson, J. A., & Nothnick, W. B. (2019) · Molecular Human Reproduction · doi:10.1093/molehr/gaz065 · Cited by 17
“sion of cyclooxygenase-2 (Bulun et al., 2012), while activation of ESR2 induces expression of several factors associated with endometriosis pathophysiology, including macrophage migration inhibitory factor”
BackgroundXiao, L. Y., Pei, T., Huang, W., Zhou, M., Fu, J., Tan, J., Liu, T., Song, Y., & Yang, S. (2020) · PLoS ONE · doi:10.1371/journal.pone.0234086 · Cited by 17
Gut Microbiota Dysbiosis in Endometriosis: A Potential Link to Inflammation and Disease Progression
Baușic, A., Scurtu, F., Manu, A., Matasariu, D., & Brătilă, E. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26115144 · Cited by 18
“By favouring a chronic inflammatory and hyperoestrogenic environment, the microbiota plays a role in the development of endometriosis [32].”
Émond, J.-P., Caron, P., Pušić, M. N., Turcotte, V., Simonyan, D., Vogler, A., Osredkar, J., Rižner, T. L., & Guillemette, C. (2023) · Frontiers in Endocrinology · doi:10.3389/fendo.2022.1034614 · Cited by 18
Korzekwa, A. J., Bah, M. M., Gęstwicka, M., Socha, B. M., & Skarzynski, D. J. (2012) · Theriogenology · doi:10.1016/j.theriogenology.2012.09.023 · Cited by 16
Notch activity mediates oestrogen-induced stromal cell invasion in endometriosis
Li, N., Zhang, L., Li, Q., Du, Y., Liu, H., Liu, Y., & Xiong, W. (2018) · Reproduction · doi:10.1530/rep-18-0326 · Cited by 16
Saare, M., Krigul, K. L., Laisk, T., Ponandai‐Srinivasan, S., Rahmioğlu, N., Kumar, P. G. L., Zondervan, K. T., Salumets, A., & Peters, M. (2018) · Biology of Reproduction · doi:10.1093/biolre/ioy067 · Cited by 17
Eisalou, M. Y., & Farahpour, M. R. (2022) · Scientific Reports · doi:10.1038/s41598-022-06883-4 · Cited by 15
Andersen, C. L., Boisen, M. M., Sikora, M. J., Ma, T., Tseng, G. C., Suryawanshi, S., Vlad, A., Elishaev, E., Edwards, R. P., & Oesterreich, S. (2018) · Hormones and Cancer · doi:10.1007/s12672-018-0350-9 · Cited by 15
Nasiri, N., Babaei, S., Moini, A., & Eftekhari‐Yazdi, P. (2021) · Journal of Reproduction & Infertility · doi:10.18502/jri.v22i4.7648 · Cited by 15
“which form positive feedback and support both the induction and persistence of inflammation followed by fibrosis, pelvic pain, and infertility (21, 22).”
BackgroundKim, H. J., Kim, S. H., Oh, Y. S., Lee, S. R., & Chae, H. D. (2022) · Biomedicines · doi:10.3390/biomedicines10112992 · Cited by 15
Peritoneal autoantibody profiling identifies p53 as an autoantibody target in endometriosis
Harden, S. L., Tan, T. Y., Ku, C. W., Zhou, J., Chen, Q., Chan, J. K. Y., Brosens, J. J., & Lee, Y. H. (2023) · Fertility and Sterility · doi:10.1016/j.fertnstert.2023.02.025 · Cited by 14
Kataoka, H., Mori, T., Okimura, H., Matsushima, H., Ito, F., Koshiba, A., Tanaka, Y., Akiyama, K., Maeda, E., Sugahara, T., et al. (2019) · Human Reproduction · doi:10.1093/humrep/dez067 · Cited by 14
“ERβ was previously shown to directly bind to ERα promoter and repress ERα expression, leading to a state of progesterone resistance in endometriosis (Bulun et al., 2012).”
BackgroundA current view of the role of epigenetic changes in the aetiopathogenesis of endometriosis
Kokcu, A. (2016) · Journal of Obstetrics and Gynaecology · doi:10.3109/01443615.2015.1036403 · Cited by 13
“ER β simulates prostaglandin E2 (PGE2) production in endometriotic tissues and cells via inducing cyclooxygenase-2 or COX2 expression (Bulun et al. 2012).”
BackgroundNon-Hormonal Strategies in Endometriosis: Targets with Future Clinical Potential
Ramos‐Niño, M. E. (2025) · Journal of Clinical Medicine · doi:10.3390/jcm14145091 · Cited by 16
“ER β promotes gene expression related to inflammation but reduces progesterone receptor levels, which creates progesterone resistance that characterizes endometriosis [39].”
Endometriosis and comorbidities: molecular mechanisms and clinical implications
Petraglia, F., Vannuccini, S., Donati, C., Jeljeli, M. M., Bourdon, M., & Chapron, C. (2025) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2025.09.002 · Cited by 23
Eldafira, E., Prasasty, V. D., ABINAWANTO, A., Syahfirdi, L., & Pujianto, D. A. (2020) · Turkish Journal of Pharmaceutical Sciences · doi:10.4274/tjps.galenos.2019.94914 · Cited by 14
Relationship between triglyceride-glucose index and endometriosis: a cross-sectional analysis
Cao, Y., Yang, Q., Mai, Q., Wuliu, J., & Deng, K. (2024) · BMC Women s Health · doi:10.1186/s12905-024-03287-6 · Cited by 15
Managing the neuroinflammatory pain of endometriosis in light of chronic pelvic pain
Pergolizzi, J. V., LeQuang, J. A., Coluzzi, F., El-Tallawy, S. N., Magnusson, P., Ahmed, R. S., Varrassi, G., & Porpora, M. G. (2024) · Expert Opinion on Pharmacotherapy · doi:10.1080/14656566.2024.2425727 · Cited by 15
“Macrophages can promote endometrial tissue adhesion, which it has been suggested might create ECMs of endometrial cells capable of proliferation [20,83].”
Comparing endometriotic lesions with eutopic endometrium: time to shift focus?
Colgrave, E. M., Keast, J. R., Bittinger, S. E., Healey, M., Rogers, P. A. W., Holdsworth‐Carson, S. J., & Girling, J. E. (2021) · Human Reproduction · doi:10.1093/humrep/deab208 · Cited by 13
The role of progesterone receptor membrane component (PGRMC) in the endometrium
Velázquez-Hernández, D. M., Vázquez-Martínez, E. R., & Camacho‐Arroyo, I. (2022) · Steroids · doi:10.1016/j.steroids.2022.109040 · Cited by 14
Bulun, S. E. (2019) · Elsevier eBooks · doi:10.1016/b978-0-323-47912-7.00025-1 · Cited by 14
Self-citationYoshino, O., Suzukamo, Y., Yoshihara, K., & Takahashi, N. (2022) · Advances in Therapy · doi:10.1007/s12325-022-02301-3 · Cited by 14
Kılıço, İ., Kökçü, A., Kefeli, M., et al. (2013) · Gynecologic and Obstetric Investigation · doi:10.1159/000356686 · Cited by 13
Wu, L., Lan, D.-T., Sun, B., Su, R. J., Pei, F., Kuang, Z., Su, Y., Lin, S., Wang, X., Zhang, S., et al. (2024) · Journal of Ethnopharmacology · doi:10.1016/j.jep.2024.118659 · Cited by 12
Liu, Y.-N., Hu, X.-J., Liu, B., Shang, Y.-J., Xu, W.-T., & Zhou, H.-F. (2021) · Evidence-Based Complementary and Alternative Medicine · doi:10.1155/2021/4521843 · Cited by 14
FoxA2 represses ERβ-mediated pyroptosis in endometriosis by transcriptionally inhibiting IGF2BP1
Feng, Y., Tan, B., Dong, H., & Zheng, L. (2023) · Experimental Cell Research · doi:10.1016/j.yexcr.2023.113539 · Cited by 12
SULFATION PATHWAYS: Contribution of intracrine oestrogens to the aetiology of endometriosis
Piccinato, C. D. A., Malvezzi, H., Gibson, D. A., & Saunders, P. T. K. (2018) · Journal of Molecular Endocrinology · doi:10.1530/jme-17-0297 · Cited by 12
Distinct molecular pathways in ovarian endometrioid adenocarcinoma with concurrent endometriosis
Zhang, C., Wang, X., Anaya, Y., Parodi, L., Cheng, L., Anderson, M. L., & Hawkins, S. M. (2018) · International Journal of Cancer · doi:10.1002/ijc.31768 · Cited by 12
Chiappini, F., Ceballos, L., Olivares, C., Bastón, J. I., Miret, N., Pontillo, C., Zárate, L., Singla, J. J., Farina, M., Meresman, G., et al. (2022) · Food and Chemical Toxicology · doi:10.1016/j.fct.2022.112867 · Cited by 11
The endocrine aspects of endometriosis
Petraglia, F., Vannuccini, S., Dolmans, M., Speciale, A. R., Bourdon, M., Marcellin, L., Donnez, J., & Chapron, C. (2025) · European Journal of Endocrinology · doi:10.1093/ejendo/lvaf192 · Cited by 13
Patiño-García, D., Palomino, J., Pomés, C., Celle, C., Torres-Estay, V. A., & Orellana, R. (2023) · Biomedicines · doi:10.3390/biomedicines11041169 · Cited by 12
“A significant increase in ERα or reduction in ERβ levels can be considered as a beneficial effect for endometriosis treatment [5,15,26,37].”
BackgroundKim, J., Cha, S., Lee, M. Y., et al. (2019) · Development & Reproduction · doi:10.12717/dr.2019.23.3.263 · Cited by 11
An Analysis of ESR2 and CYP19A1 Gene Expression Levels in Women With Endometriosis
SZAFLIK, T., SMOLARZ, B., MROCZKOWSKA, B., KULIG, B., SOJA, M., ROMANOWICZ, H., BRYŚ, M., FORMA, E., & SZYŁŁO, K. (2020) · In Vivo · doi:10.21873/invivo.11970 · Cited by 11
Hertlein, L., Rath, J., Zeder-Göß, C., Fürst, S. T., Bayer, D., Trillsch, F., Mahner, S., Burges, A., & Jeschke, U. (2017) · Oncology Letters · doi:10.3892/ol.2017.6592 · Cited by 11
“In ectopic endometrial lesions and AM, it has been reported that high levels of ERβ expression, 100-times higher than that in eutopic endometrium, may be detected (15).”
BackgroundHRT in Women Undergoing Pelvic Clearance for Endometriosis—A Case Report and a National Survey
Amer, S., & Bazmi, S. (2023) · Journal of Clinical Medicine · doi:10.3390/jcm12010336 · Cited by 11
“Furthermore, the highly expressed oestrogen in endometriotic tissue is present in its most biologically active form [14,15].”
BackgroundCheng, Y.-H., Huang, C., Lien, H.-T., Hsiao, Y.-Y., Weng, P.-L., Chang, Y.-C., Cheng, J., & Lan, K. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25073873 · Cited by 10
“The ER β gene plays a role in modulating the inflammasome and apoptosis complexes in the pathogenesis of endometriosis [124,126].”
BackgroundEpithelial-to-mesenchymal transition in the development of adenomyosis
Huang, B., Tsai, H., Wang, P., Twu, N.-F., Yen, M., & Chen, Y. (2015) · Gynecology and Minimally Invasive Therapy · doi:10.1016/j.gmit.2015.05.002 · Cited by 10
Sutrisno, S., Wulandari, R. C. L., Sulistyowati, D. W. W., Wulandari, R. F., Wahyuni, E. S., Yueniwati, Y., & Santoso, S. (2015) · Asian Pacific Journal of Reproduction · doi:10.1016/s2305-0500(15)30003-8 · Cited by 11
Estetrol Inhibits Endometriosis Development in an In Vivo Murine Model
Zabala, A. S., Conforti, R. A., Delsouc, M. B., Filippa, V., Guevara, M. M. M., Giannini, A., Simoncini, T., Vallcaneras, S. S., & Casais, M. (2024) · Biomolecules · doi:10.3390/biom14050580 · Cited by 10
“It is expected that the findings showed in the present preclinical study may serve to support the aforementioned studies as well as those to be developed in the future.”
BackgroundResultLu, F.-F., Wang, Z., Yang, Q., Yan, F.-S., Xu, C., Wang, M.-T., Xu, Z.-J., Cai, S.-Y., & Guan, R. (2024) · Frontiers in Endocrinology · doi:10.3389/fendo.2024.1438079 · Cited by 10
Physiological and Pathological Roles of Estrogen Receptor
Korach, K. S., Hewitt, S. C., Hamilton, K. J., Li, Y., Ramsey, J. T., Garcia, M., Mathura, E., & Arao, Y. (2018) · Cancer drug discovery and develogment/Cancer drug discovery and development · doi:10.1007/978-3-319-99350-8_2 · Cited by 10
The role of gut dysbiosis in endometriosis’ diagnosis and treatment approaches – case report
Baușic, A., Crețoiu, S., Bauşic, V., Matasariu, D., Stănculescu, R., & Brătilă, E. (2023) · Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie · doi:10.47162/rjme.64.2.17 · Cited by 6
“Microbiota contributes to the development of EM by promoting a longlasting inflammatory and hyperestrogenic environment [23, 24].”
BackgroundMazur, E. C., Large, M. J., & DeMayo, F. J. (2014) · Elsevier eBooks · doi:10.1016/b978-0-12-397175-3.00024-7 · Cited by 10
Steroids receptors immunohistochemical expression in different sites of endometriosis
Massarotti, C., Badenier, I. M., Paudice, M., et al. (2020) · Journal of Gynecology Obstetrics and Human Reproduction · doi:10.1016/j.jogoh.2020.101861 · Cited by 9
Sun, J., Gan, L., & Sun, J. (2022) · Genes · doi:10.3390/genes14010086 · Cited by 9
“ClusterB was revealed to be associated with significantly overexpressed VEGFA and VEGFC and, notably, downregulated ESR1 and PGR, which are characteristic biomarkers of endometriosis [33], indicating that clusterB might be highly linked to endometriosis [30].”
BackgroundInfluentialSutrisno, S., Mariyani, M., Herawati, I., Rinata, E., Jehanara, J., Yueniwati, Y., Nurdiana, N., Noorhamdani, N., & Santoso, S. (2014) · Asian Pacific Journal of Reproduction · doi:10.1016/s2305-0500(14)60043-9 · Cited by 9
Chaichian, S., Firoozabadi, Z. D., Rokhgireh, S., Tahermanesh, K., Mehdizadehkashi, A., Govahi, A., Minaeian, S., Mehdizadeh, M., & Ajdary, M. (2024) · BMC Women s Health · doi:10.1186/s12905-024-03095-y · Cited by 11
“It affects approximately 10% of women of reproductive age, with a higher prevalence observed among women aged 20–50 experiencing chronic pelvic pain and infertility [1].”
BackgroundAssociations between Estrogen Receptor Gene Polymorphisms and Endometriosis
Mun, M. J., Kim, J.-H., Kim, T.-H., Hwang, J., & Jang, W. C. (2013) · Journal of Menopausal Medicine · doi:10.6118/jksm.2013.19.2.64 · Cited by 8
Lu, R., Zhu, J., Li, X., Zeng, C., Huang, Y., Peng, C., Zhou, Y., & Xue, Q. (2024) · Journal of genetics and genomics/Journal of Genetics and Genomics · doi:10.1016/j.jgg.2023.12.012 · Cited by 9
Self-citationAn update on endometriosis biomarkers
Le, K., NEZHAT, C. R., Nezhat, C., Benor, A. Z., & DeCherney, A. H. (2024) · Minerva Obstetrics and Gynecology · doi:10.23736/s2724-606x.23.05369-1 · Cited by 9
Immune pathway through endometriosis to ovarian cancer
Calmon, M. S., Lemos, F. F. B., Luz, M. S., Pinheiro, S. L. R., Silva, L. G. D. O., Santos, G. L. C., Rocha, G. R., & de Melo, F. F. (2024) · World Journal of Clinical Oncology · doi:10.5306/wjco.v15.i4.496 · Cited by 10
Polymorphisms in the 3′UTR Region of ESR2 and CYP19A1 Genes in Women with Endometriosis
Szaflik, T., Smolarz, B., Romanowicz, H., Bryś, M., Forma, E., & Szyłło, K. (2020) · European Journal of Obstetrics & Gynecology and Reproductive Biology · doi:10.1016/j.ejogrb.2020.05.023 · Cited by 8
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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-09-28, under version 3 of the claim definition (prompt extract-v3).
A second model labelled each claim on 2026-09-28 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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