ArticleNature medicine2012
A new isoform of steroid receptor coactivator-1 is crucial for pathogenic progression of endometriosis.
Article in Nature medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 1 of them a synthesis that pooled it.
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Who cites it
86 citing papers in PubMed, 1 synthesis or guideline pooled it, 144 citations in OpenAlex.
- Pharmaceuticals targeting signaling pathways of endometriosis as potential new medical treatment: A review.Medicinal research reviews · 2021Pooled it
- Urine, peritoneal fluid and omental fat proteomes of reproductive age women: Endometriosis-related changes and associations with endocrine disrupting chemicals.Journal of proteomics · 2015Trial
- Steroid receptor coactivators: from basic research to translational opportunities.Endocrine reviews · 2026Review
- Comprehensive transcript and protein profiling reveals ERα rather than ERβ as the predominant estrogen receptor in human endometriotic lesions.Communications biology · 2026Article
- A Biomedical Researcher's Guide for Analyzing Short Tandem Repeat (STR) Genotypes of Human Cell Lines and in Vitro Tissue Samples Using Three Standard Authentication Algorithms.Current protocols · 2026Article
- Hormonal Dysregulation and Neuroinflammation in Endometriosis: Convergent Druggable Pathways.Current issues in molecular biology · 2026Review
- Nuclear factor IX promotes endometriosis progression through transcriptional activation of tetraspanin-2.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Identifying Predictive Biomarkers and Immune Infiltration Features in Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2026Article
- miR-130b-5p Regulates Expression of ERβ via IGFBP2/SREBP1 Axis in Human Endometriotic Stromal Cells.Reproductive sciences (Thousand Oaks, Calif.) · 2026Article
- From Mice to Primates: Assessing Hormone-Based Endometriosis Models for Preclinical and Therapeutic Insights.Iranian journal of medical sciences · 2025Review
- Targeting steroid receptor coactivators for the treatment of benign female reproductive disorders.Endocrine connections · 2025Review
- Polychlorinated Biphenyls Alter Estrogen Receptor β-mediated Epigenetic Regulation, Promoting Endometriosis.Endocrinology · 2025Article
- Polychlorinated biphenyl Endocrine Disruptor Alters Estrogen Receptor beta-Mediated Epigenetic Regulation, Promoting Endometriosis.Research square · 2025Article
- Insights into the Molecular Mechanisms and Signaling Pathways of Epithelial to Mesenchymal Transition (EMT) in the Pathophysiology of Endometriosis.International journal of molecular sciences · 2025Review
- The inconsistent pathogenesis of endometriosis and adenomyosis: insights from endometrial metabolome and microbiome.mSystems · 2025Article
- Polychlorinated Biphenyl-126 Activates AXL/ERb/DNMT3A Axis to Drive Endometriosis Progression.Research square · 2025Article
- A long journey to the discovery of nuclear receptor coactivator existence, physiology, pathology, and therapy.The Journal of biological chemistry · 2025Article
- Immune pathway through endometriosis to ovarian cancer.World journal of clinical oncology · 2024Review
- Transgenic mice applications in the study of endometriosis pathogenesis.Frontiers in cell and developmental biology · 2024Review
- Potential Significance of Serum Autoantibodies to Endometrial Antigens, α-Enolase and Hormones in Non-Invasive Diagnosis and Pathogenesis of Endometriosis.International journal of molecular sciences · 2023Article
26 more citing papers are in PubMed but not listed here.
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9 authors at 1 institution in 1 country.
Funding
Abstract
Endometriosis is considered to be an estrogen-dependent inflammatory disease, but its etiology is unclear. Thus far, a mechanistic role for steroid receptor coactivators (SRCs) in the progression of endometriosis has not been elucidated. An SRC-1-null mouse model reveals that the mouse SRC-1 gene has an essential role in endometriosis progression. Notably, a previously unidentified 70-kDa SRC-1 proteolytic isoform is highly elevated both in the endometriotic tissue of mice with surgically induced endometriosis and in endometriotic stromal cells biopsied from patients with endometriosis compared to normal endometrium. Tnf⁻/⁻ and Mmp9⁻/⁻ mice with surgically induced endometriosis showed that activation of tumor necrosis factor a (TNF-α)-induced matrix metallopeptidase 9 (MMP9) activity mediates formation of the 70-kDa SRC-1 C-terminal isoform in endometriotic mouse tissue. In contrast to full-length SRC-1, the endometriotic 70-kDa SRC-1 C-terminal fragment prevents TNF-α-mediated apoptosis in human endometrial epithelial cells and causes the epithelial-mesenchymal transition and the invasion of human endometrial cells that are hallmarks of progressive endometriosis. Collectively, the newly identified TNF-α-MMP9-SRC-1 isoform functional axis promotes pathogenic progression of endometriosis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.