The DOI matches its Crossref record; 51 of the 51 references it cites were found in a registry or an index.
Estrogen Receptor β Modulates Apoptosis Complexes and the Inflammasome to Drive the Pathogenesis of Endometriosis
Open accessAbstract
Alterations in estrogen-mediated cellular signaling play an essential role in the pathogenesis of endometriosis. In addition to higher estrogen receptor (ER) β levels, enhanced ERβ activity was detected in endometriotic tissues, and the inhibition of enhanced ERβ activity by an ERβ-selective antagonist suppressed mouse ectopic lesion growth. Notably, gain of ERβ function stimulated the progression of endometriosis. As a mechanism to evade endogenous immune surveillance for cell survival, ERβ interacts with cellular apoptotic machinery in the cytoplasm to inhibit TNF-α-induced apoptosis. ERβ also interacts with components of the cytoplasmic inflammasome to increase interleukin-1β and thus enhance its cellular adhesion and proliferation properties. Furthermore, this gain of ERβ function enhances epithelial-mesenchymal transition signaling, thereby increasing the invasion activity of endometriotic tissues for establishment of ectopic lesions. Collectively, we reveal how endometrial tissue generated by retrograde menstruation can escape immune surveillance and develop into sustained ectopic lesions via gain of ERβ function.
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In the citing paper
“Aberrantly high ESR2 levels regulate several pathological processes in endometriotic tissue including proliferation, inhibition of apoptosis, inflammation and pain transmission”
From Endometriosis and nuclear receptors (2019) · cites this paper as Han et al., 2015
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“The inhibition of ESR2 activity by an ESR2-selective estrogen antagonist suppresses lesion growth in these animals, whereas gain of ESR2 function stimulates the progression of endometriosis”
From Endometriosis and nuclear receptors (2019) · cites this paper as Han et al., 2015
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 [8]
In the citing paper
“Progesterone resistance may of course explain this unexpected issue [18,19,20,21,22].”
From Endometriosis and Medical Therapy: From Progestogens to Progesterone Resistance to GnRH Antagonists: A Review (2021) · cites this paper as [19]
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Metadata
- Authors
- Han, S. J., Jung, S. Y., Wu, S.-P., Hawkins, S. M., Park, M. J., Kyo, S., Qin, J., Lydon, J. P., Tsai, S. Y., Tsai, M.-J., DeMayo, F. J., & O’Malley, B. W.
- Affiliations
- Baylor College of Medicine (US)
- Kanazawa University (JP)
- Corresponding author
- O’Malley, Bert W.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2015-11
- Volume
- 163
- Issue
- 4
- Pages
- 960-974
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC4640214
- OpenAlex
- W2169528901
- Cited by
- 380
- References
- 51
- Citations by year
- 2026: 29 · 2025: 40 · 2024: 42 · 2023: 47 · 2022: 40 · 2021: 41 · 2020: 42 · 2019: 38 · 2018: 28 · 2017: 15 · 2016: 17 · 2015: 1
- FWCI
- 23.20
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (P30CA123125)
- National Institute of Diabetes and Digestive and Kidney Diseases (U19 DK-62434, P01DK059820, U19DK062434)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (U54 HD-0077495, R01HD082786, R01HD07857, R01HD08188, U54HD007495, R01HD042311, R03HD077495, K12HD050128, R01HD008188, R01HD007857)
- 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 › Ectopic Pregnancy Diagnosis and Management
- Keywords
- endometriosis, estrogen receptor beta, apoptosis, inflammasome, IL-1β, TNF-induced apoptosis, epithelial-mesenchymal transition, immune evasion, retrograde menstruation, ectopic lesions
- MeSH terms
- Animals, Cell Adhesion, Endometriosis, Female, Humans, Immunologic Surveillance, Menstruation, Tumor Necrosis Factor-alpha, Apoptosis, Estrogen Receptor alpha, Estrogen Receptor beta, Cell Proliferation, Mice, Interleukin-1beta, Inflammasomes
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.
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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