ArticleClinical epigenetics2018
Article in Clinical epigenetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
40 citing papers in PubMed, 94 citations in OpenAlex.
- Epigenetic vulnerability in endocrine disruption: bridging mechanisms, models, and environmental inequities.Clinical epigenetics · 2026Review
- Endocrine Disruptors in Child Obesity and Related Disorders: Early Critical Windows of Exposure.Current nutrition reports · 2025Review
- Maternal Nutrition, Toxicants, and Epigenetic Programming of Obesity Across Generations.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Review
- Review
- Maternal Exposure to Low-Dose BDE-47 Induced Weight Gain and Impaired Insulin Sensitivity in the Offspring.International journal of molecular sciences · 2024Article
- Prenatal exposure to environmental phenols and phthalates and altered patterns of DNA methylation in childhood.Environment international · 2024Article
- Interindividual differences of dietary fat-inducible Mest in white adipose tissue of C57BL/6J mice are not heritable.Obesity (Silver Spring, Md.) · 2024Article
- Childhood obesity from the genes to the epigenome.Frontiers in endocrinology · 2024Review
- (Micro)Plastics Are Toxic Pollutants.Toxics · 2023Review
- The State of Research and Weight of Evidence on the Epigenetic Effects of Bisphenol A.International journal of molecular sciences · 2023Article
- Re-evaluation of the risks to public health related to the presence of bisphenol A (BPA) in foodstuffs.EFSA journal. European Food Safety Authority · 2023Article
- Current Evidence on Bisphenol A Exposure and the Molecular Mechanism Involved in Related Pathological Conditions.Pharmaceutics · 2023Review
- Inherited Epigenetic Hallmarks of Childhood Obesity Derived from Prenatal Exposure to Obesogens.International journal of environmental research and public health · 2023Review
- Modulation of fetoplacental growth, development and reproductive function by endocrine disrupters.Frontiers in endocrinology · 2023Review
- TheToxicology reports · 2023Article
- Fetal exposure to phthalates and bisphenols and DNA methylation at birth: the Generation R Study.Clinical epigenetics · 2022Article
- Natural Products in Mitigation of Bisphenol A Toxicity: Future Therapeutic Use.Molecules (Basel, Switzerland) · 2022Review
- An Interplay between Epigenetics and Translation in Oocyte Maturation and Embryo Development: Assisted Reproduction Perspective.Biomedicines · 2022Review
- Potential Pro-Tumorigenic Effect of Bisphenol A in Breast Cancer via Altering the Tumor Microenvironment.Cancers · 2022Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
24 authors at 9 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Exposure to endocrine-disrupting chemicals can alter normal physiology and increase susceptibility to non-communicable diseases like obesity. Especially the prenatal and early postnatal period is highly vulnerable to adverse effects by environmental exposure, promoting developmental reprogramming by epigenetic alterations. To obtain a deeper insight into the role of prenatal bisphenol A (BPA) exposure in children's overweight development, we combine epidemiological data with experimental models and BPA-dependent DNA methylation changes. Methods: BPA concentrations were measured in maternal urine samples of the LINA mother-child-study obtained during pregnancy ( Results: In prenatally BPA-exposed children two CpG sites with deviating cord blood DNA-methylation profiles were identified, among them a hypo-methylated CpG in the promoter of the obesity-associated mesoderm-specific transcript ( Conclusions: Our study provides evidence that
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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.