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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In the paper
“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
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 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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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
“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.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- 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.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- 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.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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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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- Load-bearing: fails — The paper’s conclusions may not depend on it.
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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.
- Based: passes — The paper gives a reason why it holds.
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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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
“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.
- Checkable: passes — It can be checked against evidence.
- 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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Cited by
Sorted by citations
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Endometriosis: pathogenesis and treatment
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“Conversely, ERβwas reported overexpressed, determining an inversion of ERβ to ERα ratio as compared to eutopic endometrium [91].”
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“…and mutations; (ii) an altered steroid hormone balance or responsiveness as estrogens have been linked to the pathogenesis of gynecological cancers (Bulun et al., 2012); (iii) iron-associated oxidative stress, currently considered the most important trigger, being able to attack ‘fragile’ sites in…”
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Hormonal treatments for endometriosis: The endocrine background
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“In terms of alterations in ERs activity, an overexpression of ERβ and a downregulation of ERα [39, 40] have been observed in endometriosis.”
BackgroundEstrogen Receptors and Endometriosis
Chantalat, É., Valera, M., Vaysse, C., Noirrit‐Esclassan, E., Rusidzé, M., Weyl, A., Vergriete, K., Buscail, É., Lluel, P., Fontaine, C., et al. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21082815 · Cited by 335
Endometriosis: hormone regulation and clinical consequences of chemotaxis and apoptosis
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“One of the putative factors responsible for higher Akt phosphorylation in endometriotic cells may be the continuous local stimulation of ERs due to intralesional production of estradiol, as suggested by studies showing local expression of aromatase (Bulun et al., 2012).”
BackgroundEndometriosis and nuclear receptors
Yilmaz, B. D., & Bulun, S. E. (2019) · Human Reproduction Update · doi:10.1093/humupd/dmz005 · Cited by 243
“…PGR isoforms increase throughout the proliferative phase and peak before ovulation under the influence of increasing estrogen levels; in endometriosis, PGR levels remain very low to undetectable, possibly due to an abnormally low ESR1: ESR2 ratio in endometriotic stromal cells (Bulun et al., 2012).”
BackgroundSelf-citationEstrogen Receptor Function: Impact on the Human Endometrium
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“Compared with endometrial tissue, ERb mRNA and protein levels were more than 100-fold increased, while the levels of ERa were several times lower (98); inhibiting the enhanced ERb activity via an”
BackgroundPathogenetic Mechanisms of Deep Infiltrating Endometriosis
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“Endometriosis cells highly express vascular endothelial growth factor (VEGF) and this is increased in red vascular peritoneal endometriotic lesions compared to older black or white scarred lesions.49 The angiogenic characteristics of endometriotic lesions appear to differ between SPE, OMA, and DIE.”
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Self-citationPeripheral changes in endometriosis-associated pain
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“Estrogens have been shown to support the growth and inflammation processes in endometriotic lesions (Bulun et al., 2012).”
Regulation of Inflammation Pathways and Inflammasome by Sex Steroid Hormones in Endometriosis
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“Recently, to investigate the role of non-genomic activation of ER-β in this disease, a mouse model of surgically induced endometriosis was used through autotransplantation of fragments of endometrial tissue in the peritoneal cavity, both in mice with overexpression of ER-β (ERβ-OE) and in ERβ-null mice.”
BackgroundInfluentialGreaves, E., Cousins, F., Murray, A., Esnal-Zufiaurre, A., Fassbender, A., Horne, A., & Saunders, P. (2014) · American Journal of Pathology · doi:10.1016/j.ajpath.2014.03.011 · Cited by 170
Endometriosis: where are we and where are we going?
Greene, A. D., Lang, S. A., Kendziorski, J. A., Sroga-Rios, J. M., Herzog, T. J., & Burns, K. A. (2016) · Reproduction · doi:10.1530/rep-16-0052 · Cited by 187
Dual suppression of estrogenic and inflammatory activities for targeting of endometriosis
Zhao, Y., Gong, P., Chen, Y., Nwachukwu, J. C., Srinivasan, S., Ko, C., Bagchi, M. K., Taylor, R. N., Korach, K. S., Nettles, K. W., et al. (2015) · Science Translational Medicine · doi:10.1126/scitranslmed.3010626 · Cited by 170
Epithelial-to-mesenchymal transition in the development of endometriosis
Yang, Y., & Yang, W. (2017) · Oncotarget · doi:10.18632/oncotarget.16472 · Cited by 171
“In the previous studies, people believed that whether of ovarian or peritoneal locations, had higher ERβ expression rather than ERα compared with normal human endometrial cells [48], which was similarly detected in many animal models of endometriosis [49, 50].”
ResultLocal and systemic factors and implantation: what is the evidence?
Fox, C. W., Morin, S. J., Jeong, J., Scott, R. T., & Lessey, B. A. (2016) · Fertility and Sterility · doi:10.1016/j.fertnstert.2016.02.018 · Cited by 170
Cyclooxygenase-2 in Endometriosis
Lai, Z., Yang, H., Ha, S., Chang, K., Mei, J., Zhou, W.-J., Qiu, X., Wang, X.-Q., Zhu, R., Li, D., et al. (2019) · International Journal of Biological Sciences · doi:10.7150/ijbs.35128 · Cited by 176
Diet and endometriosis risk: A literature review
Parazzini, F., Viganò, P., Candiani, M., & Fedele, L. (2013) · Reproductive BioMedicine Online · doi:10.1016/j.rbmo.2012.12.011 · Cited by 165
The management of menopause in women with a history of endometriosis: A systematic review
Gemmell, L. C., Webster, K. E., Kirtley, S., Vincent, K., Zondervan, K. T., & Becker, C. M. (2017) · Human Reproduction Update · doi:10.1093/humupd/dmx011 · Cited by 154
“This expression profile results in locally elevated levels of the biologically active form of oestrogen (oestradiol) (Kitawaki et al., 2002; Bulun et al., 2012).”
BackgroundBurns, K. A., Rodriguez, K., Hewitt, S., Janardhan, K., Young, S., & Korach, K. (2012) · Endocrinology · doi:10.1210/en.2012-1294 · Cited by 143
Estrogen receptor β: the guardian of the endometrium
Hapangama, D. K., Kamal, A. M., & Bulmer, J. N. (2015) · Human Reproduction Update · doi:10.1093/humupd/dmu053 · Cited by 145
Gou, Y., Li, X., Li, P., Zhang, H., Xu, T., Wang, H., Wang, B., Ma, X., Xue, J., & Zhang, Z. (2019) · Human Reproduction · doi:10.1093/humrep/dez019 · Cited by 133
Di-(2-ethylhexyl)-phthalate induces oxidative stress in human endometrial stromal cells in vitro
Cho, Y. J., Park, S. B., & Han, M. S. (2015) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2015.03.003 · Cited by 132
Treatment of pain associated with deep endometriosis: alternatives and evidence
Ferrero, S., Alessandri, F., Racca, A., & Maggiore, U. L. R. (2015) · Fertility and Sterility · doi:10.1016/j.fertnstert.2015.08.031 · Cited by 124
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Zhou, S., Yi, T., Liu, R., Bian, C., Qi, X., He, X., Wang, K., Li, J., Zhao, X., Huang, C., et al. (2012) · Molecular & Cellular Proteomics · doi:10.1074/mcp.m112.017988 · Cited by 113
The Role of Peritoneal Macrophages in Endometriosis
Ramírez-Pavez, T. N., Martinez‐Esparza, M., Ruiz‐Alcaraz, A. J., Marín‐Sánchez, P., Machado‐Linde, F., & García–Peñarrubia, P. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms221910792 · Cited by 113
“This, in conjunction with the increased expression of ERβ [127] in both ovarian and peritoneal lesions, could over-activate estrogen-dependent signaling pathways in endometrial tissues, stimulating its corresponding biological effects.”
BackgroundLiu, X., Zhang, Q., & Guo, S.-W. (2018) · Reproductive Sciences · doi:10.1177/1933719117718275 · Cited by 110
Ovarian hormones-autophagy-immunity axis in menstruation and endometriosis
Shen, H., Zhang, T., Yang, H., Lai, Z., Zhou, W., Mei, J., Shi, J., Zhu, R., Xu, F., Li, D., et al. (2021) · Theranostics · doi:10.7150/thno.55241 · Cited by 107
Han, S. J., & O’Malley, B. W. (2014) · Human Reproduction Update · doi:10.1093/humupd/dmu002 · Cited by 98
“Interestingly, elevated ERb enhances progesterone resistance in endometriotic tissues (Bulun et al., 2012).”
BackgroundIs it time for a paradigm shift in drug research and development in endometriosis/adenomyosis?
Guo, S., & Groothuis, P. G. (2018) · Human Reproduction Update · doi:10.1093/humupd/dmy020 · Cited by 93
“…investigators demonstrated that ERβ expression is strongly elevated in endometriotic tissue as a result of demethylation of the gene promoter region (Bulun et al., 2012), and that ERβ, binding to estradiol with the same affinity as ERα, could be a key player in the pathophysiology of endometriosis.”
BackgroundThree Types of Endometriosis: Pathogenesis, Diagnosis and Treatment. State of the Art
Imperiale, L., Nisolle, M., Noël, J., & Fastrez, M. (2023) · Journal of Clinical Medicine · doi:10.3390/jcm12030994 · Cited by 110
“Endometriotic lesions show an increased expression of aromatase, estrogen receptor β, and steroidogenic acute regulatory protein [16] and decreased expression of 17β-hydroxysteroid dehydrogenase 2 [17].”
BackgroundHammarstrand, S., Jakobsson, K., Andersson, E., Xu, Y., Li, Y., Olovsson, M. H., & Andersson, E. M. (2021) · Environment International · doi:10.1016/j.envint.2021.106819 · Cited by 93
“Whereas both uterine leiomyoma and endometriosis are estrogen-dependent diseases (Borahay et al., 2017; Bulun et al., 2012), PCOS is characterized by an excess of androgens, in particular testosterone (Escobar-Morreale 2018).”
BackgroundJones, R. L., Tanadini‐Lang, S., Kendziorski, J. A., Greene, A., & Burns, K. A. (2018) · Environmental Health Perspectives · doi:10.1289/ehp3802 · Cited by 88
“We further examined expression levels of genes known to be involved in endometriosis (Bukulmez et al. 2008; Bulun et al. 2012; Chang et al. 2011; Osteen et al. 2003): Estrogen Receptor 1 and 2 ( Esr1, Esr2 ), Matrix Metallopeptidase 9 ( Mmp9 ), Matrix Metallopepti-dase 7 ( Mmp7 ), and Mucin 4 (…”
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Aromatase and endometriosis: estrogens play a role
Ferrero, S., Remorgida, V., Maganza, C., Venturini, P. L., Salvatore, S., Papaleo, E., Candiani, M., & Maggiore, U. L. R. (2014) · Annals of the New York Academy of Sciences · doi:10.1111/nyas.12411 · Cited by 84
Exploring diagnostic m6A regulators in endometriosis
Jiang, L., Zhang, M., Wu, J., Wang, S., Xiang, Y., Yi, M., Zhang, X., & Fang, X. (2020) · Aging · doi:10.18632/aging.202163 · Cited by 83
“However, the ‘protagonist’ in EMs is thought to be ESR2 (ESRβ); the preferential expression of this gene would reduce the expression level of ESR1 in endometriotic stromal cells [32].”
BackgroundEndometriosis-Associated Angiogenesis and Anti-angiogenic Therapy for Endometriosis
Chung, M. S., & Han, S. J. (2022) · Frontiers in Global Women s Health · doi:10.3389/fgwh.2022.856316 · Cited by 93
“Furthermore, women with endometriosis display significantly elevated levels of ERβ in ovarian endometrioma when compared to normal endometrium (125).”
BackgroundRole of nuclear receptors in blastocyst implantation
Vasquez, Y. M., & DeMayo, F. J. (2013) · Seminars in Cell and Developmental Biology · doi:10.1016/j.semcdb.2013.08.004 · Cited by 82
Altered genome-wide methylation in endometriosis
Naqvi, H., Ilagan, Y., Krikun, G., & Taylor, H. S. (2014) · Reproductive Sciences · doi:10.1177/1933719114532841 · Cited by 82
“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) Higher expression of estrogen receptor amplifies estrogenic effects and the proliferative capacity of endometrial cells.”
BackgroundPolyphenols as a Diet Therapy Concept for Endometriosis—Current Opinion and Future Perspectives
Gołąbek-Grenda, A., Kowalska, K., & Olejnik, A. M. (2021) · Nutrients · doi:10.3390/nu13041347 · Cited by 97
“These are ovaries, which primarily convert cholesterol to estradiol and secrete it periodically into the circulation, peripheral tissues such as the adipose tissue and skin, that convert androstenedione to estrone in relatively small quantities, and endometriotic tissue, synthesizing de novo high amounts of estradiol…”
BackgroundIncreased Association Between Endometriosis and Endometrial Cancer
Yu, H.-C., Lin, C.-Y., Chang, W., Shen, B., Chang, W.-P., & Chuang, C.-M. (2015) · International Journal of Gynecological Cancer · doi:10.1097/igc.0000000000000384 · Cited by 82
Daidzein-rich isoflavone aglycones inhibit cell growth and inflammation in endometriosis
Takaoka, O., Mori, T., Ito, F., Okimura, H., Kataoka, H., Tanaka, Y., Koshiba, A., Kusuki, I., Shigehiro, S., Amami, T., et al. (2018) · The Journal of Steroid Biochemistry and Molecular Biology · doi:10.1016/j.jsbmb.2018.04.004 · Cited by 81
Minireview: Steroid-Regulated Paracrine Mechanisms Controlling Implantation
Pawar, S., Hantak, A. M., Bagchi, I. C., & Bagchi, M. K. (2014) · Molecular Endocrinology · doi:10.1210/me.2014-1074 · Cited by 82
“Bulun et al (103) have shown that specific steroid hormone receptor isoforms are differentially regulated in stromal cells isolated from normal and endometriotic tissue.”
BackgroundRole of Oxidative Stress in Epigenetic Modification in Endometriosis
Ito, F., Yamada, Y., 重光, 愛., Akinishi, M., Kaniwa, H., Miyake, R., Yamanaka, S., & Kobayashi, H. (2017) · Reproductive Sciences · doi:10.1177/1933719117704909 · Cited by 79
Challenges in endometriosis miRNA studies — From tissue heterogeneity to disease specific miRNAs
Saare, M., Rekker, K., Laisk, T., Rahmioğlu, N., Zondervan, K. T., Salumets, A., Götte, M., & Peters, M. (2017) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2017.06.018 · Cited by 77
da Silva, D. M., Gross, L. A., Neto, E. D. P. G., Lessey, B. A., & Savaris, R. F. (2017) · Journal of the Endocrine Society · doi:10.1210/js.2017-00053 · Cited by 83
Androgens, oestrogens and endometrium: a fine balance between perfection and pathology
Gibson, D. A., Simitsidellis, I., Collins, F., & Saunders, P. T. K. (2020) · Journal of Endocrinology · doi:10.1530/joe-20-0106 · Cited by 76
MAP kinases and the inflammatory signaling cascade as targets for the treatment of endometriosis?
Santulli, P., Marcellin, L., Tosti, C., Chouzenoux, S., Cerles, O., Borghese, B., Batteux, F., & Chapron, C. (2015) · Expert Opinion on Therapeutic Targets · doi:10.1517/14728222.2015.1090974 · Cited by 75
Estradiol promotes EMT in endometriosis via MALAT1/miR200s sponge function
Du, Y., Zhang, Z., Xiong, W., Li, N., Liu, H., He, H., Li, Q., Liu, Y., & Zhang, L. (2018) · Reproduction · doi:10.1530/rep-18-0424 · Cited by 73
Bruner‐Tran, K. L., Mokshagundam, S., Herington, J. L., Ding, T., & Osteen, K. G. (2018) · Current Women s Health Reviews · doi:10.2174/1573404813666170921162041 · Cited by 80
The role of mitogen‐activated protein kinase signaling pathway in endometriosis
Bora, G., & Yaba, A. (2021) · Journal of obstetrics and gynaecology research · doi:10.1111/jog.14710 · Cited by 73
Transvaginal Elastosonography as an Imaging Technique for Diagnosing Adenomyosis
Liu, X., Ding, D., Ren, Y., & Guo, S. (2018) · Reproductive Sciences · doi:10.1177/1933719117750752 · Cited by 78
Zhang, B., Zhou, W., Gu, C., Wu, K., Yang, H., Mei, J., Yu, J.-J., Hou, X.-F., Sun, J., Xu, F., et al. (2018) · Cell Death and Disease · doi:10.1038/s41419-018-0581-2 · Cited by 71
Endometriosis and cardiovascular disease
Marchandot, B., Curtiaud, A., Matsushita, K., Trimaille, A., Host, A., Faller, É., Garbin, O., Akladios, C. Y., Jesel, L., & Morel, O. (2022) · European Heart Journal Open · doi:10.1093/ehjopen/oeac001 · Cited by 74
NLRP3 inflammasome: a new therapeutic target for high-risk reproductive disorders?
Zhou, F., Li, C., & Zhang, S. (2020) · Chinese Medical Journal · doi:10.1097/cm9.0000000000001214 · Cited by 71
Endometriosis: Update of Pathophysiology, (Epi) Genetic and Environmental Involvement
Monnin, N., Fattet, A.-J., & Koscinski, I. (2023) · Biomedicines · doi:10.3390/biomedicines11030978 · Cited by 79
“ESR and SF-1 receptors epigenetic modifications in endometriosis [4,22,23].”
BackgroundEndometriosis and the Fallopian Tubes: Theories of Origin and Clinical Implications
Hill, C. J., Fakhreldin, M., Maclean, A., Dobson, L., Nancarrow, L., Bradfield, A., Choi, F., Daley, D., Tempest, N., & Hapangama, D. K. (2020) · Journal of Clinical Medicine · doi:10.3390/jcm9061905 · Cited by 70
“The pathological overexpression of ERβ, considered to be the result of deficient methylation of the ERβ promoter, stimulates both inflammation [44,45] and loss of PR expression [46].”
BackgroundEndometrial Intracrinology: Oestrogens, Androgens and Endometrial Disorders
Gibson, D. A., Simitsidellis, I., Collins, F., & Saunders, P. T. K. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19103276 · Cited by 70
“Examples include epithelial cell expression of AR in endometrial cancers [26] and upregulation of ERbeta in endometriosis [35].”
BackgroundThe known, the unknown and the future of the pathophysiology of endometriosis
Ochoa Bernal, M. A., & Fazleabas, A. T. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25115815 · Cited by 59
“…of ESR2 in human Several studies have reported lower levels of ESR1 and higher levels of ESR2 in human endometriotic tissues and primary stromal cells compared with endometrial tissue and cells [55]. endometriotic tissues and primary stromal cells compared with endometrial tissue and cells [55].”
BackgroundPaola, R. D., Fusco, R., Gugliandolo, E., Crupi, R., Evangelista, M., Granese, R., & Cuzzocrea, S. (2016) · Frontiers in Pharmacology · doi:10.3389/fphar.2016.00382 · Cited by 59
“…tissue of patients affected by disease; in particular elevated expression of Extrogen receptor β is predicted to play a role in the development of endometriosis; probably, it contributes to the resistance to progesterone action in some of patients suffering from endometriosis (Bulun et al., 2012).”
BackgroundNothnick, W. B., & Alali, Z. (2016) · F1000Research · doi:10.12688/f1000research.7504.1 · Cited by 55
Stress, pain, anxiety, and depression in endometriosis–Targeting glial activation and inflammation
Mokhtari, T., Irandoost, E., & Sheikhbahaei, F. (2024) · International Immunopharmacology · doi:10.1016/j.intimp.2024.111942 · Cited by 59
Structure, Function, and Evaluation of the Female Reproductive Tract
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Epigenetic Modulation of Collagen 1A1: Therapeutic Implications in Fibrosis and Endometriosis1
Zheng, Y., Khan, Z., Zanfagnin, V., Correa, L. F., Delaney, A. A., & Daftary, G. S. (2016) · Biology of Reproduction · doi:10.1095/biolreprod.115.138115 · Cited by 50
Endometriosis and autoimmunity
Blanco, L. P., Salmeri, N., Temkin, S. M., Shanmugam, V. K., & Stratton, P. (2025) · Autoimmunity Reviews · doi:10.1016/j.autrev.2025.103752 · Cited by 59
Epigenetic Factors in Eutopic Endometrium in Women with Endometriosis and Infertility
Adamczyk, M., Wender-Ożegowska, E., & Kędzia, M. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23073804 · Cited by 51
“Endometriotic implants comprise stromal cells whose epigenetic pattern is similar to the phenotype of thecal and granulosa ovarian cells and tissue macrophages [64,65].”
Vercellini, P., Bandini, V., Viganò, P., Stefano, G. D., Merli, C. E. M., & Somigliana, E. (2023) · Human Reproduction · doi:10.1093/humrep/dead229 · Cited by 50
“…in endometriosis, as E2 is crucial for endometrial gland survival, with subsequent production of a number of inflammatory molecules leading to peritoneal and subperitoneal tissue remodelling, adhesions, and fibrosis (Bulun et al. , 2012, 2019; Reis et al. , 2013; Clemenza et al. , 2022).”
Reversal of fortune: estrogen receptor-β in endometriosis
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“locations, display higher ERβ expression compared with normal human endometrial cells; this was not shown for ERα (Bulun et al. 2012).”
BackgroundCao, Y., Zhuang, M., Yang, Y., et al. (2014) · Evidence-based Complementary and Alternative Medicine · doi:10.1155/2014/781684 · Cited by 45
“The past researches suggested that estrogen took effect only through the single and classic ERα, and with the discovery of ERβ, more evidence indicates that the pathophysiology mechanism of estrogen to target cells is regulated by ERα and ERβ [12].”
BackgroundLe, N., Cregger, M. A., Brown, V. A., de Mola, J. R. L., Bremer, P., Nguyen, L., Groesch, K. A., Wilson, T. S., Díaz‐Sylvester, P., & Braundmeier‐Fleming, A. (2021) · PLoS ONE · doi:10.1371/journal.pone.0261362 · Cited by 45
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Role of tight junctions in signal transduction: an update
Takano, K., Kojima, T., Sawada, N., & Himi, T. (2014) · Europe PMC (PubMed Central) · doi:10.17877/de290r-7042 · Cited by 44
“tors (Bulun et al., 2012).”
BackgroundDysfunctional signaling underlying endometriosis: current state of knowledge
Cho, Y. J., Lee, S. H., Park, J. W., Han, M. S., Park, M. J., & Han, S. J. (2018) · Journal of Molecular Endocrinology · doi:10.1530/jme-17-0227 · Cited by 49
Yang, M., Jiang, C., Chen, H., Nian, Y., Zhimiao, B., & Ha, C. (2015) · Reproductive Biology and Endocrinology · doi:10.1186/s12958-015-0090-4 · Cited by 43
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Developmental Toxicant Exposure Is Associated with Transgenerational Adenomyosis in a Murine Model
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Targeting YAP1 ameliorates progesterone resistance in endometriosis
Lin, S., Li, W., Lin, S.-C., Hou, H.-T., Tsai, Y.-C., Lin, T.-C., Wu, M., & Tsai, S. (2023) · Human Reproduction · doi:10.1093/humrep/dead071 · Cited by 38
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Dyson, M. T., Kakinuma, T., Pavone, M. E., Monsivais, D., Navarro, A., Malpani, S. S., Ono, M., & Bulun, S. E. (2015) · Fertility and Sterility · doi:10.1016/j.fertnstert.2015.06.046 · Cited by 37
Self-citationEffect of simvastatin on baboon endometriosis†
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The role of Lipoxin A4 in endometrial biology and endometriosis
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Link between Endometriosis, Atherosclerotic Cardiovascular Disease, and the Health of Women Midlife
Taşkın, Ö., Rikhraj, K. J. K., Tan, J., Sedlak, T., Rowe, T., & Bedaiwy, M. A. (2019) · Journal of Minimally Invasive Gynecology · doi:10.1016/j.jmig.2019.02.022 · Cited by 37
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“Cyclooxygenase 2 (COX-2), encoded by PTGS2, plays an important role in the development of endometriosis [24].”
BackgroundAdvances in targeting estrogen synthesis and receptors in patients with endometriosis
Clemenza, S., Vannuccini, S., Ruotolo, A., Capezzuoli, T., & Petraglia, F. (2022) · Expert Opinion on Investigational Drugs · doi:10.1080/13543784.2022.2152325 · Cited by 34
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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