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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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
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.
- Based: passes — The paper gives a reason why it holds.
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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.
- Checkable: passes — It can be checked against evidence.
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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.
- Checkable: passes — It can be checked against evidence.
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- 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
“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 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]
Citations
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From Inflammation to Malignancy: The Link Between Endometriosis and Gynecological Cancers
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“A severely high ERβ-to-ERα ratio in endometriotic stromal cells is associated with suppressed PR, contributing to progesterone resistance (37).”
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Estrogen and progesterone receptors in endometriosis
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“The estrogen-dependence of endometriosis may be partially responsible for better HRQoL in older EACPP patients, due to declining estrogen levels taming disease [13, 14].”
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Diseases of the genitourinary system
Nesterova, A. P., Климов, Е. А., Zharkova, M., Sozin, S., Sobolev, V. V., Ivanikova, N. V., Shkrob, M., & Yuryev, A. (2019) · Elsevier eBooks · doi:10.1016/b978-0-12-817086-1.00013-0 · Cited by 4
Proestling, K., Schreiber, M., Miedl, H., Hudson, Q. J., Husslein, H., Kuessel, L., Gstoettner, M., Wenzl, R. J., & Yotova, I. (2024) · Biomedicines · doi:10.3390/biomedicines12081657 · Cited by 3
“When established, endometriosis lesions are characterized by estrogen dominance caused by the local estrogen production and altered ER signaling, presenting an overexpression of ESR2 and a downregulation of ESR1 [43,44].”
BackgroundCell Communication in Endometrium: Understanding and Improving Endometrial Biomarkers
Kshersagar, J. R., Damle, M. N., Sharma, R. K., & Joshi, M. G. (2025) · Advances in experimental medicine and biology · doi:10.1007/5584_2025_867 · Cited by 4
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Therapeutic Potential of Herbal Compounds in Curing Dysmenorrhea Naturally: A Review
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Gene Expression in Endometriosis
Joshi, N., Su, R., & Fazleabas, A. T. (2019) · Springer eBooks · doi:10.1007/978-3-030-28584-5_11 · Cited by 3
Targeting Mast Cells as a Viable Therapeutic Option in Endometriosis
Hart, D. A. (2017) · EMJ Reproductive Health · doi:10.33590/emjreprohealth/10314034 · Cited by 3
Single-cell characterization of menstrual fluid at homeostasis and in endometriosisPreprint
Schwalie, P. C., Bafligil, C., Russeil, J., Zachara, M., Biočanin, M., Alpern, D., Aasna, E., Deplancke, B., Canny, G., & Gonçalves, Â. (2024) · eLife · doi:10.7554/elife.99558 · Cited by 3
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Is exercise duration more important than intensity in endometriosis?
Hartmann, T. E., Baker, K. A., & Girard, D. (2025) · BMC Women s Health · doi:10.1186/s12905-025-04160-w · Cited by 3
“Estradiol, the biologically active form of estrogen, may aggravate the pathological processes by elevating inflammation, facilitating endometrial growth thereby increasing symptom severity [7].”
Endometriosis and Endometriosis-Associated Tumors
Simmen, R. C. M., Quick, C. M., & Zheng, W. (2024) · Springer eBooks · doi:10.1007/978-981-19-7696-4_12-1 · Cited by 2
Hormones and Inflammation: An Update on Endometriosis
Pavone, D., Turrini, I., Sorbi, F., Vannuccini, S., Capezzuoli, T., Fambrini, M., & Petraglia, F. (2019) · ISGE series · doi:10.1007/978-3-030-14358-9_14 · Cited by 2
Mystery of endometriosis — catamenial pneumothorax
Svidinskaya, E. A., Lysenko, A. V., & Brykin, G. V. (2022) · Pirogov Russian Journal of Surgery · doi:10.17116/hirurgia2022041110 · Cited by 3
Akad, M., Socolov, R. V., Covali, R. A., Catalina Daniela, S. T. A. N., Crauciuc, E., Popovici, D., Stan, C. I., Akad, F., & Socolov, D. G. (2022) · MAEDICA – a Journal of Clinical Medicine · doi:10.26574/maedica.2022.17.3.557 · Cited by 3
Monist, M. J., Lewkowicz, D., Jóźwik, M., Gogacz, M., Bogusiewicz, M., Rechberger, T., & Semczuk, A. (2019) · Case Reports in Oncology · doi:10.1159/000499760 · Cited by 3
The Association between Endometriosis and Immunological diseasesPreprint
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. (2024) · medRxiv · doi:10.1101/2024.07.08.24310092 · Cited by 2
Effectiveness of hysterectomy in endometriosis treatment
Jaiswal, A., Dube, A. S., Kaushik, J., Upadhayay, K., & Kushwaha, A. (2024) · International Journal of Scientific Reports · doi:10.18203/issn.2454-2156.intjscirep20243807 · Cited by 1
Yang, J., Li, P.-T., & Xi, S.-Y. (2025) · Discover Oncology · doi:10.1007/s12672-025-02887-4 · Cited by 1
“As an estrogen-dependent chronic inflammatory disorder, molecular alterations in estrogen signaling and inflammatory pathways facilitate both implantation and proliferation of abnormal endometrial tissue [7].”
Baek, J. K., Lee, J. K., Chung, Y. S., & Seo, S. K. (2025) · Microorganisms · doi:10.3390/microorganisms13092144 · Cited by 1
“This observation is consistent with prior animal studies where ER β antagonism led to partial reduction in lesion growth but failed to completely inhibit proliferation [18,23].”
Xu, S., Xin, Y., Lv, F., Hu, X., & Xiao, R.-P. (2026) · Chinese Science Bulletin (Chinese Version) · doi:10.1360/csb-2025-5885 · Cited by 1
“子宫内膜异位症 ( 简称内异症 , endometriosis) [43,44] 是一种慢性炎症性的妇科疾病 , 其本质为子宫内膜样 组织在宫腔外异位生长 , 常见于盆腔内器官 , 如卵巢和 腹膜 , 也可侵犯肠道、膀胱等邻近结构 , 甚至异位至盆 腔外 [45] .”
Kralj, S., Zeman, K., Mikuš, M., Karačić, A., Pršo, A.-M. L., Ćorić, M., & Renko, I. (2026) · Trials · doi:10.1186/s13063-025-09405-5 · Cited by 3
“Its pathophysiology is highly complex and includes intertwined hormonal and inflammatory mechanisms [5, 6].”
Nemeti, G. I., Craciun, A. E., Măgureanu, D. C., Militaru, F. C., Bocșan, I. C., Crăciun, C.-I., Rusu, A., Melincovici, C. S., Buzoianu, A. D., Mureșan, D., et al. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27114883 · Cited by 3
Estole-Casanova, L. A. (2023) · Acta Medica Philippina · doi:10.47895/amp.vi0.6994 · Cited by 1
Crop and pesticide effects on gut microbiota and neurological functions: a review
Komura, T., Yoshida, M., & Nishikawa, Y. (2024) · Exploration of neuroscience · doi:10.37349/en.2024.00038 · Cited by 1
Wang, J., Liang, Y., Liang, X., Peng, H., Wang, Y., Xu, M., Liang, X., Yao, H., Liu, X., Zeng, L., et al. (2024) · Frontiers in Pharmacology · doi:10.3389/fphar.2024.1426660 · Cited by 1
A Primer on Clinical Classification and Pathophysiology of Endometriosis
Mishra, A., & Modi, D. (2024) · Fertility Science and Research · doi:10.25259/fsr_7_2024 · Cited by 1
Sherwani, S., Khan, M. W. A., Khan, W. A., et al. (2024) · Frontiers in Oncology · doi:10.3389/fonc.2024.1493320 · Cited by 1
Transcription factor addictions: exploring the potential Achilles’ Heel of endometriosis
Yang, Y., Du, Y., Ma, X., Yuan, G., Li, G., Zhang, Q., & Zhou, S. (2025) · Science China Life Sciences · doi:10.1007/s11427-024-2832-8 · Cited by 1
“Moreover, a decrease in the ER α -to-ER β ratio contributes to perturbed E2 induction of PGR expression (Bulun et al., 2012).”
Endometriosis: causas, histopatogenia y epidemiología en México y el mundo
Luna, A. G., Ruiz, R. P., Álvarez, D. M., Rojas, R. M. L., & Vásquez, A. G. L. (2013) · Revista Mexicana de Medicina de la Reproducción · Cited by 1
An Overview of Epigenetic Correlates of Human Chronic Pain Conditions
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Heat Shock Proteins (HSP) in Stress-Related Inflammatory Diseases
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Elevated phosphorylation of estrogen receptor α at serine-118 in ovarian endometrioma
Sun, H. J., Hirata, T., Koga, K., Arakawa, T., Nagashima, N., Neriishi, K., Elsherbini, M., Maki, E., Izumi, G., Harada, M., et al. (2022) · F&S Science · doi:10.1016/j.xfss.2022.04.004 · Cited by 1
Single-cell characterization of menstrual fluid at homeostasis and in endometriosisPreprint
Schwalie, P. C., Bafligil, C., Russeil, J., Zachara, M., Biočanin, M., Alpern, D., Aasna, E., Deplancke, B., Canny, G., & Gonçalves, Â. (2024) · eLife · doi:10.7554/elife.99558.1 · Cited by 1
Neue Aspekte zur Ätiologie und Pathogenese der Endometriose
Wölfler, M. M., Klein, P., Zalewski, M., & Maass, N. (2015) · Der Gynäkologe · doi:10.1007/s00129-014-3422-0
Pain related genes in endometriosis: A meta-analysis
Saxena, M. (2015) · The Sydney eScholarship Repository (The University of Sydney)
Review article: ROLE OF TIGHT JUNCTIONS IN SIGNAL TRANSDUCTION: AN UPDATE
Takano, K., Kojima, T., Sawada, N., & Himi, T. (2015)
Venegas, S., Parada, E., Boric, M. A., Hugo Sovino, S., Fuentes, A., Gabler, F., González-Ramos, R., & Johnson, M. C. (2015) · Open Journal of Obstetrics and Gynecology · doi:10.4236/ojog.2015.57060
“In addition, the known estrogenic microenvironment in eutopic and ectopic endometria in women with endometriosis [3] [34]-[36] may be also involved in the induction of the NGF expression in macrophages as Kanda et al.”
BackgroundNoninflammatory Tumor-Like Changes of the Gallbladder
Zimmermann, A. (2016) · Springer eBooks · doi:10.1007/978-3-319-26956-6_159
Russu, M. C. (2019) · IntechOpen eBooks · doi:10.5772/intechopen.84203
Endometriosis and Endometriosis-Associated Tumors
Simmen, R. C. M., Quick, C. M., Kelley, A. S., & Zheng, W. (2019) · Springer eBooks · doi:10.1007/978-981-13-3019-3_12
Bragança, C. M. C. (2013) · Portuguese National Funding Agency for Science, Research and Technology (RCAAP Project by FCT) · doi:10.34626/2fxe-we94
Rolla, E. D. (2021) · Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature · doi:10.3410/f.740035280.793585488
Noninflammatory Tumor-Like Changes of the Gallbladder
Zimmermann, A. (2016) · Springer eBooks · doi:10.1007/978-3-319-26587-2_159-1
Cieri‐Hutcherson, N. E., Carden, D., & Hutcherson, T. C. (2017) · The American Pharmacists Association eBooks · doi:10.21019/pharmacotherapyfirst.endometriosis_overview
Hikmah, R., Hendarto, H., & Widjiati, W. (2022) · Majalah Obstetri & Ginekologi · doi:10.20473/mog.v30i12022.1-9
The Role of Platelets in the Pathogenesis of Endometriosis and New Therapeutic Ideas
许, 万. (2022) · Advances in Clinical Medicine · doi:10.12677/acm.2022.124367
“EMT 一直被视为一种雌激素依赖性疾病。异位子宫内膜的增殖需要雌二醇，在子宫内膜异位病灶中， 雌激素受体 β (ER-β)表达明显增加[19]。另外，EMT 通常还被视为一种炎性疾病，在其病灶促炎因子激 活环氧合酶 2 (COX-2)，导致前列腺素 E2 (PGE2)的产生增加，进而刺激类固醇生成急性调节蛋白、芳香 酶、17β-羟基类固醇脱氢酶 1 型(HSD17B1)等部分产生 E2 的关键基因，导致雌激素 E2 的增加。增加的 E2 进一步刺激雌激素受体 β (ER-β)，进一步诱导 COX-2 增加[20]。已有研究表明，活化的血小板不仅可 以通过上调 StAR、HSD3B2、芳香酶和 HSD17B1 的基因表达，从而使子宫…”
Influentialvan Trotsenburg, M., Luikenaar, R. A. C., & Meriggiola, M. C. (2022) · Cambridge University Press eBooks · doi:10.1017/9781108899987.012
Benign Gynecological Conditions in Transgender and Gender Diverse People
van Trotsenburg, M., Meriggiola, M. C., & Luikenaar, R. A. C. (2022) · Cambridge University Press eBooks · doi:10.1017/9781108899987.015
Primary Umbilical Endometriosis Coexisting with Multiple Uterine Myomas : A Rare Case ReportPreprint
Nongo, B. H., & Isah, D. A. (2023) · Research Square · doi:10.21203/rs.3.rs-3121760/v1
Bakun, O. V., & Yuzko, O. M. (2023) · Clinical anatomy and operative surgery · doi:10.24061/1727-0847.22.1.2023.03
“Hypothyroidism, susceptibility to vaginal candidiasis, auto-immune diseases, fibromyalgia, chronic fatigue syndrome, headaches, arthralgias and myalgias, asthma and allergies are more common comorbidities in women with endometriosis than in women without it [1].”
BackgroundHosseini, E., Shahhosseini, M., Afsharian, P., Mehraein, F., Ashrafi, M., & Aflatoonian, R. (2023) · Armaghane Danesh · doi:10.61186/armaghanj.28.5.7
Lu, F.-F., Wang, Z., Yang, Q., et al. (2024) · Research Square · doi:10.21203/rs.3.rs-4207495/v1
Single-cell characterization of menstrual fluid at homeostasis and in endometriosisPreprint
Schwalie, P. C., Bafligil, C., Russeil, J., Zachara, M., Biočanin, M., Alpern, D., Aasna, E., Deplancke, B., Canny, G., & Gonçalves, Â. (2024) · medRxiv · doi:10.1101/2024.05.06.24306766
“Likewise, among genes downregulated in endometriosis patients we found an enrichment for targets of estrogen receptor alpha ( ESR1 ), whose expression has been previously found to be suppressed in endometric stromal cells (30).”
BackgroundEndometriosis: Pathogenesis, Diagnosis and Treatment, volume II
(2024) · Frontiers research topics · doi:10.3389/978-2-8325-4894-3
Rashidpour, F., Farzanegi, P., & Abbaszadeh, H. (2023) · شهباز. · doi:10.61186/mlj.17.2.26
Yamane, E., Azuma, Y., Matsumoto, M., Sato, E., Ota, Y., Harada, T., & Taniguchi, F. (2024) · American Journal of Reproductive Immunology · doi:10.1111/aji.70010
Ding, Y., Yang, X., Wei, Q., et al. (2024) · Frontiers in Pharmacology · doi:10.3389/fphar.2024.1492098
“This leads to a positive feedback loop, enhancing estrogen production and in fl ammation, which further promotes the EMS progression (Bulun et al., 2012; Takaoka et al., 2018).”
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Azurocidin is Associated with Dienogest-resistance in Ovarian Endometriotic Cysts
Watanabe, M., Kobayashi, Y., Ishida, M., Tajima, A., Tanigaki, S., & Morisada, T. (2025) · Reproductive Sciences · doi:10.1007/s43032-025-01795-w
Deng, J. F., Li, J., Xu, L., & Yi, T. (2025) · Archives of Gynecology and Obstetrics · doi:10.1007/s00404-025-08025-3
“In contrast, endometriosis tissues exhibit significantly elevated estrogen receptor beta (ER-β)—over 100-fold higher compared to normal endometrial tissue—and reduced PR expression [22].”
Endometriosis and Endometriosis-Associated Tumors
Simmen, R. C. M., Quick, C. M., & Zheng, W. (2025) · Springer eBooks · doi:10.1007/978-981-97-4822-8_12
Heath, A. E., Zuend, C. F., Goodman, W. A., Koyutürk, M., & Brubaker, D. K. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.09.15.676330
“I ncreased ERβ expression has been proposed as a key driver of increased estrogen signaling and diminished progesterone responsiveness in endometriotic lesions (36).”
The Role of Hysterectomy in the Management of Endometriosis
Afuape, N. O. (2025) · Seminars in Reproductive Medicine · doi:10.1055/s-0045-1813017
Vallée, A., & Ayoubi, J.-M. (2026) · PLoS ONE · doi:10.1371/journal.pone.0329110
“This estrogen excess may further stimulate the growth and inflammatory response of ectopic endometrial tissue, worsening endometriosis symptoms such as pelvic pain and dyspareunia [39,40].”
Sympathetic neural control of blood pressure across the premenopausal lifespan
Saboune, J., Boyes, N. G., Limberg, J. K., & Usselman, C. W. (2026) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00739.2025
Damm, G. K., Zhang, F., Koentgen, S., Jayawardana, T. C., Houshyar, Y., Read, S., Condous, G., El‐Assaad, F., & Hold, G. L. (2026) · iScience · doi:10.1016/j.isci.2026.115437
“10,11 Nearly a decade later, research found changes in the gut microbiota signatures of endometriosis patients compared to healthy controls, showing reduced microbial richness, a common disease biomarker 8,12,13 as well as increased numbers of pathogens and decreased protective bacteria in…”
Analyse des micro-ARN dans le cadre de l'endométriose : apport clinico-biologique
Dabi, Y. (2023) · theses.fr (ABES) · doi:10.70675/ee221eccza824z4ddezbeb8z04286230c430
Berlanda, N., Bandini, V., Croci, G. A., Dridi, D., Nobili, M. V., Cipriani, S., & Vercellini, P. (2026) · Human Reproduction · doi:10.1093/humrep/deag059
Adenomyosis and Endometriosis: Two Faces of the Same Disease?
Socolov, R. V., Păvăleanu, I., Socolov, D. G., Toma, L. M., & Pruteanu, A. I. (2026) · Obstetrics and gynecology. · doi:10.5772/intechopen.1014688
Devabhaktuni, P., Yelamanchi, S. D., & Singh, M. (2026) · International Journal of Reproduction Contraception Obstetrics and Gynecology · doi:10.18203/2320-1770.ijrcog20261480
Cancer-like Hallmarks of Endometriosis: The Role of Estrogen Signaling and Stem Cell Plasticity
Signorile, P. G., Baldi, A., Mazzotti, A., Montanaro, M., & Boccellino, M. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27104510 · Cited by 1
“Its reduced expression in ectopic lesions leads to an altered transcriptional response to estrogen, favoring ER β -driven signaling pathways that promote cell survival, inflammation, and tissue invasion [20,21].”
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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