ArticleThe Journal of clinical endocrinology and metabolism2015
Decreased Notch pathway signaling in the endometrium of women with endometriosis impairs decidualization.
Article in The Journal of clinical endocrinology and metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
What it found
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Who cites it
66 citing papers in PubMed, 130 citations in OpenAlex.
- Intrauterine human chorionic gonadotropin infusion in oocyte donors promotes endometrial synchrony and induction of early decidual markers for stromal survival: a randomized clinical trial.Human reproduction (Oxford, England) · 2016Trial
- Molecular Regulation of FOXO1 and Its Pathophysiological Significance in Endometriosis: A Narrative Review.Antioxidants (Basel, Switzerland) · 2025Review
- Statistical methods to disentangle genetic effects influencing infertility and early fetal viability with a genome-wide application.PLoS genetics · 2025Article
- How transcription factors regulate apoptosis in endometriosis (Review).Molecular medicine reports · 2025Review
- Balancing Decidualization, Autophagy, and Cellular Senescence for Reproductive Success in Endometriosis Biology.International journal of molecular sciences · 2025Review
- Review
- Molecular Basis of Impaired Decidualization in the Eutopic Endometrium of Endometriosis Patients.Cells · 2025Review
- Multi-omics-based mapping of decidualization resistance in patients with a history of severe preeclampsia.Nature medicine · 2025Article
- NOTCH1- and CD117-Positive Stem Cells in Human Endometriosis and Adenomyosis Lesions.Diagnostics (Basel, Switzerland) · 2024Article
- The Known, the Unknown and the Future of the Pathophysiology of Endometriosis.International journal of molecular sciences · 2024Review
- NEK2 promotes the development of ovarian endometriosis and impairs decidualization by phosphorylating FOXO1.Cellular and molecular life sciences : CMLS · 2024Article
- Notch Signaling: An Emerging Paradigm in the Pathogenesis of Reproductive Disorders and Diverse Pathological Conditions.International journal of molecular sciences · 2024Review
- Aberrant activated Notch1 promotes prostate enlargement driven by androgen signaling via disrupting mitochondrial function in mouse.Cellular and molecular life sciences : CMLS · 2024Article
- Detection of Endometriosis Lesions Using Gd-Based Collagen I Targeting Probe in Murine Models of Endometriosis.Molecular imaging and biology · 2023Article
- Expressions of Notch signalling pathway members during early pregnancy in mice.Journal of molecular histology · 2023Article
- Endometrial and placental stem cells in successful and pathological pregnancies.Journal of assisted reproduction and genetics · 2023Review
- Spheroids as a model for endometriotic lesions.JCI insight · 2023Article
- Endometrial stem/progenitor cells: Properties, origins, and functions.Genes & diseases · 2023Review
- Identification of potential biomarkers and immune infiltration characteristics in recurrent implantation failure using bioinformatics analysis.Frontiers in immunology · 2023Article
- Endometriosis Stem Cells as a Possible Main Target for Carcinogenesis of Endometriosis-Associated Ovarian Cancer (EAOC).Cancers · 2022Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
contextEndometriosis is a common gynecological disease affecting one in 10 women of reproductive age and is a major cause of pelvic pain and impaired fertility. Endometrial stromal cells of women with endometriosis exhibit a reduced response to in vitro decidualization. NOTCH1 is critical for decidualization of both mouse and human uterine stromal cells.
objectiveThis study aimed to determine whether decidualization failure in women with endometriosis is a consequence of impaired Notch signaling. SETTING AND
designWe investigated expression levels of Notch signaling components in the endometrium of women and baboons with or without endometriosis. We identified NOTCH1-regulated genes during decidualization of human uterine fibroblast (HuF) cells by microarray and quantified their expression levels in in vitro-decidualized endometrial stromal cells isolated from women with or without endometriosis.
resultsNotch signaling receptors NOTCH1 and NOTCH4, ligands JAGGED2 and DLL4, as well as direct target genes HES5 and HEY1 were decreased in the eutopic endometrium of women and baboons with endometriosis. Notch signaling was decreased in stromal cells isolated from women with endometriosis, which was associated with impaired in vitro decidualization. Genes that were down-regulated by NOTCH1 silencing in decidualized HuF cells were also decreased in decidualized endometrial stromal cells of women with endometriosis. FOXO1 acts as a downstream target of Notch signaling and endometriosis is associated with decreased expression of NOTCH1-regulated, FOXO1-responsive genes during decidualization.
conclusionsDecreased Notch signaling is associated with endometriosis and contributes to impaired decidualization through the down-regulation of FOXO1.
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What OpenQuestion holds
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.