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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In the citing paper
“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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Cites
Mutation of the mouse klotho gene leads to a syndrome resembling ageing
Kuro-o, M., Matsumura, Y., Aizawa, H., Kawaguchi, H., Suga, T., Utsugi, T., Ohyama, Y., Kurabayashi, M., Kaname, T., Kume, E., et al. (1997) · Nature · doi:10.1038/36285 · Cited by 3,837
Induction of TNF receptor I-mediated apoptosis via two sequential signaling complexes
Micheau, O., & Tschopp, J. (2003) · Cell · doi:10.1016/s0092-8674(03)00521-x · Cited by 2,738
Giudice, L. C. (2010) · New England Journal of Medicine · doi:10.1056/nejmcp1000274 · Cited by 1,924
Bulun, S. E. (2009) · New England Journal of Medicine · doi:10.1056/nejmra0804690 · Cited by 1,772
Generation and reproductive phenotypes of mice lacking estrogen receptor β
Krege, J. H., Hodgin, J. B., Couse, J. F., Enmark, E., Warner, M. N., Mahler, J. F., Sar, M., Korach, K. S., Gustafsson, J.-Α., & Smithies, O. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.26.15677 · Cited by 1,717
Eskenazi, B., & Warner, M. L. (1997) · Obstetrics and Gynecology Clinics of North America · doi:10.1016/s0889-8545(05)70302-8 · Cited by 1,617
ASK1 is required for sustained activations of JNK/p38 MAP kinases and apoptosis
Tobiume, K., Matsuzawa, A., Takahashi, T., Nishitoh, H., Morita, K., Takeda, K., Minowa, O., Miyazono, K., Noda, T., & Ichijo, H. (2001) · EMBO Reports · doi:10.1093/embo-reports/kve046 · Cited by 1,211
Caspase‐1‐induced pyroptotic cell death
Miao, E. A., Rajan, J. V., & Aderem, A. A. (2011) · Immunological Reviews · doi:10.1111/j.1600-065x.2011.01044.x · Cited by 1,162
Impact of endometriosis on women’s lives: a qualitative study
Moradi, M., Parker, M. A., Sneddon, A., López, V., & Ellwood, D. A. (2014) · BMC Women s Health · doi:10.1186/1472-6874-14-123 · Cited by 525
Progesterone action in endometrial cancer, endometriosis, uterine fibroids, and breast cancer
Kim, J. J., Kurita, T., & Bulun, S. E. (2013) · Endocrine Reviews · doi:10.1210/er.2012-1043 · Cited by 520
Cited by
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Zondervan, K. T., Becker, C. M., & Missmer, S. A. (2020) · New England Journal of Medicine · doi:10.1056/nejmra1810764 · Cited by 2,249
Zondervan, K. T., Becker, C. M., Koga, K., Missmer, S. A., Taylor, R. N., & Viganò, P. (2018) · Nature Reviews Disease Primers · doi:10.1038/s41572-018-0008-5 · Cited by 1,257
Bulun, S. E., Yilmaz, B. D., Sison, C., Miyazaki, K., Bernardi, L., Liu, S., Kohlmeier, A., Yin, P., Milad, M., & Wei, J. (2019) · Endocrine Reviews · doi:10.1210/er.2018-00242 · Cited by 844
The Immunopathophysiology of Endometriosis
Symons, L. K., Miller, J. E., Kay, V. R., Marks, R. M., Liblik, K., Koti, M., & Tayade, C. (2018) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2018.07.004 · Cited by 601
Progesterone and Estrogen Signaling in the Endometrium: What Goes Wrong in Endometriosis?
Marquardt, R. M., Kim, T. H., Shin, J., & Jeong, J. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20153822 · Cited by 527
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
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