ReviewFrontiers in endocrinology2024
Molecular mechanism of aberrant decidualization in adenomyosis leading to reduced endometrial receptivity.
Review in Frontiers in endocrinology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Optimizing the Endometrial Factor in Recurrent Implantation Failure: From Established Diagnostics to Mechanism-Informed Management.Journal of clinical medicine · 2026Review
- Adenomyosis, Infertility and Maternal-Fetal Outcomes: Diagnostic and Therapeutic Strategies Across Disease Phenotype-A Narrative Review.Journal of clinical medicine · 2026Review
- The endometriosis-adenomyosis spectrum: shared pathophysiology and microenvironment-driven disease divergence.Reproductive biology and endocrinology : RB&E · 2026Review
- Single-cell transcriptomic landscape of the mid-secretory eutopic endometrium reveals receptivity defects in adenomyosis.Journal of translational medicine · 2026Article
- Increased Junctional Zone Stiffness and Serum Small Extracellular Vesicle Proteomic Signatures in Adenomyosis-Associated Infertility: An Exploratory SWE and Proteomic Study.International journal of women's health · 2026Article
Corrections and comments
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Authors and funding
4 authors.
Funding
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Abstract
Patients with adenomyosis not only experience a decrease in quality of life as a result of dysmenorrhea and severe monthly flow but they are also rendered infertile. Pregnancy rates are still low among women with adenomyosis, even with assisted reproduction. According to the current study, endometrial receptivity is primarily responsible for the lower conception rate among patients with adenomyosis. Decidualization of endometrial stromal cells is the fundamental requirement for endometrial receptivity and the maintenance of a normal pregnancy, even though endometrial receptivity is made up of a variety of cells, including immune cells, endometrial epithelial cells, and endometrial stromal cells. Our overview reveals that endometriosis deficiencies are present in patients with adenomyosis. These flaws may be linked to aberrant pathways in endometrial stromal cells, such as PI3K/Akt, JAK2/STAT3, and hedgehog. Correcting the abnormal expression of molecules in endometrial stromal cells in the endometrium of patients with adenomyosis may become the focus of research to improve endometrial receptivity and increase the pregnancy rate.
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