ArticleJournal of cellular and molecular medicine2014
Oestrogen-induced angiogenesis promotes adenomyosis by activating the Slug-VEGF axis in endometrial epithelial cells.
Article in Journal of cellular and molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.
- Role of angiogenesis in adenomyosis-associated abnormal uterine bleeding and subfertility: a systematic review.Human reproduction update · 2019Pooled it
- Endometriosis and Adenomyosis: Mechanotransduction, Microenvironment, and Mechanisms Beyond Lesions.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Adenomyosis, Infertility and Maternal-Fetal Outcomes: Diagnostic and Therapeutic Strategies Across Disease Phenotype-A Narrative Review.Journal of clinical medicine · 2026Review
- Review
- The interaction between inflammation and estrogen in adenomyosis : from molecular mechanisms to therapeutic strategies.Seminars in immunopathology · 2026Review
- Divergent Associations of the VEGF (Medicina (Kaunas, Lithuania) · 2026Article
- Long-term efficacy of uterine artery embolization for adenomyosis and analysis of prognostic factors: a cohort study.BMC women's health · 2026Article
- Ectopic endometrial mesenchymal stem cell-derived exosomal miR-4466 promotes angiogenesis by targeting RUNX1 in adenomyosis.Biochemistry and biophysics reports · 2026Article
- Dydrogesterone and Letrozole Combination for the Treatment of Endometriosis: A Mechanism-Based Therapeutic Approach.Obstetrics and gynecology international · 2026Article
- Endometrial Mesenchymal Stem Cell-Derived Exosomal miR-4669 Promotes EMT in Adenomyosis by Inducing M2 Macrophage Polarization via the DUSP6/ERK Pathway.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Anti-angiogenic therapy as potential treatment for adenomyosis.Angiogenesis · 2025Article
- Review
- Research Advances in Adenomyosis-Related Signaling Pathways and Promising Targets.Biomolecules · 2024Review
- The Current Understanding of Molecular Mechanisms in Adenomyosis-Associated Infertility and the Treatment Strategy for Assisted Reproductive Technology.International journal of molecular sciences · 2024Review
- Molecular Targets for Nonhormonal Treatment Based on a Multistep Process of Adenomyosis Development.Reproductive sciences (Thousand Oaks, Calif.) · 2023Review
- Exosomes: potential diagnostic markers and drug carriers for adenomyosis.Frontiers in pharmacology · 2023Review
- Pre-clinical models to study abnormal uterine bleeding (AUB).EBioMedicine · 2022Review
- Ovarian, uterine, and luteal vascular perfusions during follicular and luteal phases in the adult cyclic female rabbits with special orientation to their histological detection of hormone receptor.BMC veterinary research · 2022Article
- Increased Angiogenesis and Lymphangiogenesis in Adenomyosis Visualized by Multiplex Immunohistochemistry.International journal of molecular sciences · 2022Article
- Mechanism Study of Cinnamomi Ramulus andEvidence-based complementary and alternative medicine : eCAM · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adenomyosis is an oestrogen-dependent disease characterized by the invasion of endometrial epithelial cells into the myometrium of uterus, and angiogenesis is thought to be required for the implantation of endometrial glandular tissues during the adenomyotic pathogenesis. In this study, we demonstrate that compared with eutopic endometria, adenomyotic lesions exhibited increased vascularity as detected by sonography. Microscopically, the lesions also exhibited an oestrogen-associated elevation of microvascular density and VEGF expression in endometrial epithelial cells. We previously reported that oestrogen-induced Slug expression was critical for endometrial epithelial-mesenchymal transition and development of adenomyosis. Our present studies demonstrated that estradiol (E2) elicited a Slug-VEGF axis in endometrial epithelial cells, and also induced pro-angiogenic activity in vascular endothelial cells. The antagonizing agents against E2 or VEGF suppressed endothelial cells migration and tubal formation. Animal experiments furthermore confirmed that blockage of E2 or VEGF was efficient to attenuate the implantation of adenomyotic lesions. These results highlight the importance of oestrogen-induced angiogenesis in adenomyosis development and provide a potential strategy for treating adenomyosis through intercepting the E2-Slug-VEGF pathway.
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Registered trials
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.