ArticleActa pharmacologica Sinica2019
Hypovitaminosis D exacerbates the DNA damage load in human uterine fibroids, which is ameliorated by vitamin D3 treatment.
Article in Acta pharmacologica Sinica, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- A Systematic Review of Vitamin D and Fibroids: Pathophysiology, Prevention, and Treatment.Reproductive sciences (Thousand Oaks, Calif.) · 2023Pooled it
- Review
- Vitamin D3 ameliorates R-loop-induced replication stress and chromosomal instability in MED12-mutant uterine fibroids.Scientific reports · 2026Article
- In vivo inhibition of TDO2 in fibroids results in widespread alteration in the tumor transcriptome.Clinical science (London, England : 1979) · 2026Article
- Vitamin D and Uterine Fibroids: Insights into Pathophysiology and Therapeutic Potential.Endocrine reviews · 2026Review
- Vitamin D3 ameliorates R-loop-induced replication stress and chromosomal instability in MED12-mutant uterine fibroids.Research square · 2026Article
- Association between serum 25-hydroxyvitamin D [25(OH)D] levels and vaginal delivery in pregnant women: an observational case-control study from Türkiye.Frontiers in medicine · 2026Article
- The Potential of Vitamin D and Epigallocatechin Gallate (EGCG) for the Treatment of Uterine Fibroids: Evidence From In Vitro to Clinical Studies.Molecular nutrition & food research · 2025Review
- Nutrition and Uterine Fibroids: Clinical Impact and Emerging Therapeutic Perspectives.Journal of clinical medicine · 2025Review
- Altered extracellular matrix-related pathways accelerate the transition from normal to prefibroid myometrium in Black women.American journal of obstetrics and gynecology · 2024Article
- Emerging perspectives: unraveling the anticancer potential of vitamin DNaunyn-Schmiedeberg's archives of pharmacology · 2024Review
- The Role of Nutrition in Pathogenesis of Uterine Fibroids.Nutrients · 2023Review
- Evidence-Based Approach for Secondary Prevention of Uterine Fibroids (The ESCAPE Approach).International journal of molecular sciences · 2023Review
- The m6A reader YTHDC1-mediated lncRNA CTBP1-AS2 m6A modification accelerates cholangiocarcinoma progression.Heliyon · 2023Article
- Developmental reprogramming of myometrial stem cells by endocrine disruptor linking to risk of uterine fibroids.Cellular and molecular life sciences : CMLS · 2023Article
- Vitamin D and uterine fibroid growth, incidence, and loss: a prospective ultrasound study.Fertility and sterility · 2022Article
- Article
- Comprehensive Review of Uterine Fibroids: Developmental Origin, Pathogenesis, and Treatment.Endocrine reviews · 2022Review
- Report of Exosomes Isolated from a Human Uterine Leiomyoma Cell Line and Their Impact on Endometrial Vascular Endothelial Cells.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Dietary Natural Compounds and Vitamins as Potential Cofactors in Uterine Fibroids Growth and Development.Nutrients · 2022Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Uterine fibroids (UFs) are the most common benign neoplastic threat to women's health and associated with DNA damage and genomic instability. Hypovitaminosis D is a known risk factor for UFs, especially among African Americans. Vitamin D3 has been shown to effectively inhibit UF phenotype, but its mechanisms remain unclear. We hypothesize that Vitamin D3 ameliorates UFs by recovering the damaged DNA repair system, thus inhibits tumor progression. We compared the DNA damage status and Vitamin D receptor (VDR) expression between normal myometrial and UF primary cells. Unrepaired DNA double-strand breaks (DSBs) accumulated but VDR expression decreased in UFs. The RNA and protein levels of key DNA repair members belonging to DNA DSB sensors (MRE11, NBS1, RAD50), mediators and effectors (CHECK2, BRCA1, RAD51) were downregulated in UFs compared with myometrial cells. VDR KD induced DSB accumulation and DNA damage response (DDR) defects in myometrial cells. Using the DNA damage PCR array, the expression of many additional DNA repair genes was downregulated in VDR KD cells. Treatment of UF cells with Vitamin D3 (100 nM) significantly decreased DNA damage and restored DDR concomitant with VDR induction. Notably, the PCR array demonstrated that among 75 downregulated genes after VDR KD, 67 (89.3%) were upregulated after vitamin D3 treatment. These studies demonstrate a novel link between DNA damage and the vitamin D3/VDR axis in UFs. Vitamin D3 suppresses the UF phenotype through orchestrated targeting at multiple molecules in DNA repair pathways, thus offering novel mechanistic insights into the clinical effectiveness of vitamin D3 on UFs.
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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.