The DOI matches its Crossref record; 49 of the 49 references it cites were found in a registry or an index.
Estrogen Receptor-β, Estrogen Receptor-α, and Progesterone Resistance in Endometriosis
Open accessAbstract
Loss of progesterone signaling in the endometrium may be a causal factor in the development of endometriosis, and progesterone resistance is commonly observed in women with this disease. In endometriotic stromal cells, the levels of progesterone receptor (PR), particularly the PR-B isoform, are significantly decreased, leading to a loss of paracrine signaling. PR deficiency likely underlies the development of progesterone resistance in women with endometriosis who no longer respond to progestin therapy. Here we review the complex epigenetic and transcriptional mechanisms leading to PR deficiency. The initial event may involve deficient methylation of the estrogen receptor (ER)beta promoter resulting in pathologic overexpression of ERbeta in endometriotic stromal cells. We speculate that alterations in the relative levels of ERbeta and ERalpha in endometrial tissue dictate E2-regulated PR expression, such that a decreased ERalpha-tauomicron-ERbeta ratio may result in suppression of PR. In this review, we propose a molecular model that may be responsible for changes in ERbeta and ERalpha leading to PR loss and progesterone resistance in endometriosis.
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“This emphasizes the paramount importance of estrogen to the pathogenesis of endometriosis: estrogen promotes endometriotic cell survival, inflammation and lesion progression”
From Endometriosis and nuclear receptors (2019) · cites this paper as Bulun et al., 2010
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ERβ: Identification and characterization of a novel human estrogen receptor
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New treatment strategies and emerging drugs in endometriosis
Streuli, I., de Ziegler, D., Borghese, B., Santulli, P., Batteux, F., & Chapron, C. (2012) · Expert Opinion on Emerging Drugs · doi:10.1517/14728214.2012.668885 · Cited by 27
A 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
Metadata
- Authors
- Bulun, S., Cheng, Y.-H., Pavone, M., Xue, Q., Attar, E., Trukhacheva, E., Tokunaga, H., Utsunomiya, H., Yin, P., Luo, X., Lin, Z., Imir, G., Thung, S., Su, E., & Kim, J.
- Affiliations
- Northwestern University (US)
- Peking University (CN)
- Istanbul University-Cerrahpaşa (TR)
- Tohoku University (JP)
- Yale University (US)
- ORCID
- Venue
- Seminars in Reproductive Medicine
- Publisher
- Georg Thieme Verlag KG
- Published
- 2010-01
- Volume
- 28
- Issue
- 01
- Pages
- 036-043
- ISSN
- 1526-4564 (ISSN-L)
- 1526-8004
- PMC
- PMC3073375
- OpenAlex
- W2091204496
- Cited by
- 243
- References
- 46
- Citations by year
- 2026: 17 · 2025: 10 · 2024: 17 · 2023: 10 · 2022: 11 · 2021: 20 · 2020: 19 · 2019: 11 · 2018: 16 · 2017: 8 · 2016: 12 · 2015: 21 · 2014: 20 · 2013: 17 · 2012: 14
- FWCI
- 19.43
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Seminars in Reproductive Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (U54HD040093, HD 040093, R01HD044715)
- 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, progesterone resistance, progesterone receptor, estrogen receptor beta, estrogen receptor alpha, endometriotic stromal cells, promoter methylation, epigenetic regulation, paracrine signaling
- MeSH terms
- Endometriosis, Endometrium, Female, Humans, Progesterone, Receptors, Progesterone, Gene Expression Regulation, Neoplastic, Stromal Cells, CpG Islands, DNA Methylation, Epigenesis, Genetic, Estrogen Receptor alpha, Estrogen Receptor beta
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