ArticleInternational journal of molecular sciences2023
Epigenetic Modulation of Inflammatory Pathways in Myometrial Stem Cells and Risk of Uterine Fibroids.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
What it found
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- Causal relationship between genetically predicted uterine leiomyoma and cancer risk: a two-sample Mendelian randomization.Frontiers in endocrinology · 2024Pooled it
- Phthalate Metabolite, Mono(2-Ethyl-5-Hydroxyhexyl) Phthalate (MEHHP), Promotes Uterine-Fibroid-Associated Phenotypes in Myometrial Stem Cell-Derived 3D Organoids.Environmental toxicology · 2026Article
- Review
- Epigenetic Regulation of Uterine Smooth Muscle Tumors: Histone Modifications in Uterine Fibroids and Leiomyosarcoma.Biology · 2026Review
- Induced and spontaneous uterine leiomyomas in animal models: a scoping review.Acta cirurgica brasileira · 2026Article
- Utilising Human Myometrial and Uterine Fibroid Stem Cell-Derived Three Dimentional Organoids as a Robust Model System for Understanding the Pathophysiology of Uterine Fibroids.Cell proliferation · 2025Article
- Effect of Diethylstilbestrol on Implantation and Decidualization in Mice.International journal of molecular sciences · 2025Article
- Psychosocial Stress and MicroRNA Expression Profiles in Myometrial Tissue of Women Undergoing Surgical Treatment for Uterine Fibroids.Reproductive sciences (Thousand Oaks, Calif.) · 2024Article
- Racial disparity in uterine leiomyoma: new insights of genetic and environmental burden in myometrial cells.Molecular human reproduction · 2024Review
- Bromodomain-Containing Protein 9 Regulates Signaling Pathways and Reprograms the Epigenome in Immortalized Human Uterine Fibroid Cells.International journal of molecular sciences · 2024Article
- Evidence-Based Approach for Secondary Prevention of Uterine Fibroids (The ESCAPE Approach).International journal of molecular sciences · 2023Review
- The adverse role of endocrine disrupting chemicals in the reproductive system.Frontiers in endocrinology · 2023Review
- Endocrine-disrupting chemicals and epigenetic reprogramming in developmental origin of uterine fibroids.Science progressArticle
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
The period during which tissue and organ development occurs is particularly vulnerable to the influence of environmental exposures. However, the specific mechanisms through which biological pathways are disrupted in response to developmental insults, consequently elevating the risk of hormone-dependent diseases, such as uterine fibroids (UFs), remain poorly understood. Here, we show that developmental exposure to the endocrine-disrupting chemical (EDC), diethylstilbestrol (DES), activates the inflammatory pathways in myometrial stem cells (MMSCs), which are the origin of UFs. Significantly, the secretome of reprogrammed MMSCs enhances the expression of critical inflammation-related genes in differentiated myometrial cells through the paracrine mechanism, which amplifies pro-inflammatory and immune suppression signaling in the myometrium. The expression of reprogrammed inflammatory responsive genes (IRGs) is driven by activated mixed-lineage leukemia protein-1 (MLL1) in MMSCs. The deactivation of MLL reverses the reprogramming of IRG expression. In addition, the inhibition of histone deacetylases (HDACs) also reversed the reprogrammed IRG expression induced by EDC exposure. This work identifies the epigenetic mechanisms of MLL1/HDAC-mediated MMSC reprogramming, and EDC exposure epigenetically targets MMSCs and imparts an IRG expression pattern, which may result in a "hyper-inflammatory phenotype" and an increased hormone-dependent risk of UFs later in life.
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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.