ArticleNature communications2020
Epigenome environment interactions accelerate epigenomic aging and unlock metabolically restricted epigenetic reprogramming in adulthood.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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.
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Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- Systematic transcriptome-wide meta-analysis across endocrine disrupting chemicals reveals shared and unique liver pathways, gene networks, and disease associations.Environment international · 2024Pooled it
- ToxiTaRGET: a multi-omics database for toxicant-responsive molecular targets.Nature communications · 2026Article
- Developmental Exposure to Endocrine Disruptors and Persistent Pollutants Heightens Addiction Risk via Toxicological Mechanisms.Biomolecules & therapeutics · 2026Review
- Mapping pesticide mixtures to cancer risk at the country scale with spatial exposomics.Nature health · 2026Article
- Distinct molecular responses of human intestinal organoids to proton and photon radiation.American journal of physiology. Gastrointestinal and liver physiology · 2025Article
- Plasticity of Epigenomic and Transcriptomic Aging Reveals Common Targets for Reprogramming by Environmental Exposures.Research square · 2025Article
- Comprehensive Transcriptomic and Epigenomic Insights into Environmental Toxicant Exposures: The TaRGET II Resource.bioRxiv : the preprint server for biology · 2025Article
- Gut Microbiota Colonization in Early Life Influences Susceptibility to Adulthood Hepatic Lipid Accumulation in High-Fat-Diet-Fed Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Perinatal Exposure to Lead or Diethylhexyl Phthalate in Mice: Sex-Specific Effects on Cardiac DNA Methylation and Gene Expression across Time.Environmental health perspectives · 2025Article
- Let-7 restrains an epigenetic circuit in AT2 cells to prevent fibrogenic intermediates in pulmonary fibrosis.Nature communications · 2025Article
- Consensus on the key characteristics of metabolism disruptors.Nature reviews. Endocrinology · 2025Review
- Sex-specific associations of prenatal Chinese famine exposure with cataract risk at age sixty: a cross-sectional study.BMC women's health · 2024Article
- Transcriptomic and epigenomic signatures distinguish high- and low-risk endotypes for liver tumor development.Environmental and molecular mutagenesis · 2024Article
- Epigallocatechin Gallate for the Treatment of Benign and Malignant Gynecological Diseases-Focus on Epigenetic Mechanisms.Nutrients · 2024Review
- Persistent gene expression and DNA methylation alterations linked to carcinogenic effects of dichloroacetic acid.Frontiers in oncology · 2024Article
- Article
- NNanotoxicology · 2023Article
- Intergenerational effects of early life-stage temperature modulation on gene expression and DNA methylation in Atlantic cod (Epigenetics · 2023Article
- Identifying Novel Drug Targets for Epilepsy Through a Brain Transcriptome-Wide Association Study and Protein-Wide Association Study with Chemical-Gene-Interaction Analysis.Molecular neurobiology · 2023Article
- Developmental reprogramming of myometrial stem cells by endocrine disruptor linking to risk of uterine fibroids.Cellular and molecular life sciences : CMLS · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 1 institution in 1 country.
Funding
Abstract
Our early-life environment has a profound influence on developing organs that impacts metabolic function and determines disease susceptibility across the life-course. Using a rat model for exposure to an endocrine disrupting chemical (EDC), we show that early-life chemical exposure causes metabolic dysfunction in adulthood and reprograms histone marks in the developing liver to accelerate acquisition of an adult epigenomic signature. This epigenomic reprogramming persists long after the initial exposure, but many reprogrammed genes remain transcriptionally silent with their impact on metabolism not revealed until a later life exposure to a Western-style diet. Diet-dependent metabolic disruption was largely driven by reprogramming of the Early Growth Response 1 (EGR1) transcriptome and production of metabolites in pathways linked to cholesterol, lipid and one-carbon metabolism. These findings demonstrate the importance of epigenome:environment interactions, which early in life accelerate epigenomic aging, and later in adulthood unlock metabolically restricted epigenetic reprogramming to drive metabolic dysfunction.
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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.