ArticleEpigenetics insights2020
Sex-Specific Programming of Cardiac DNA Methylation by Developmental Phthalate Exposure.
Article in Epigenetics insights, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 27 citations in OpenAlex.
- From Exposure to Atherosclerosis: Mechanistic Insights into Phthalate-Driven Ischemic Heart Disease and Prevention Strategies.Life (Basel, Switzerland) · 2026Review
- Sex-stratified piRNA expression analysis reveals shared functional impacts of perinatal lead (Pb) exposure in murine hearts.Epigenetics · 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
- Sexually dimorphic cardiovascular impacts of prenatal exposure to a real-life environmental chemical mixture in adult offspring.Environmental toxicology and pharmacology · 2025Article
- Review
- Developmental exposures to common environmental contaminants, DEHP and lead, alter adult brain and blood hydroxymethylation in mice.Frontiers in cell and developmental biology · 2023Article
- Toxicoepigenetics and Environmental Health: Challenges and Opportunities.Chemical research in toxicology · 2022Review
- Developmental toxicant exposures and sex-specific effects on epigenetic programming and cardiovascular health across generations.Environmental epigenetics · 2022Review
- Effects of Prenatal Phthalate Exposure and Childhood Exercise on Maternal Behaviors in Female Rats at Postpartum: A Role ofInternational journal of molecular sciences · 2021Article
- Sex-Specific Alterations in Cardiac DNA Methylation in Adult Mice by Perinatal Lead Exposure.International journal of environmental research and public health · 2021Article
- Sexual Dimorphism of the Heart: Genetics, Epigenetics, and Development.Frontiers in cardiovascular medicine · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Phthalate plasticizers are ubiquitous chemicals linked to several cardiovascular diseases in animal models and humans. Despite this, the mechanisms by which phthalate exposures cause adverse cardiac health outcomes are unclear. In particular, whether phthalate exposures during pregnancy interfere with normal developmental programming of the cardiovascular system, and the resulting implications this may have for long-term disease risk, are unknown. Recent studies suggest that the effects of phthalates on metabolic and neurobehavioral outcomes are sex-specific. However, the influence of sex on cardiac susceptibility to phthalate exposures has not been investigated. One mechanism by which developmental exposures may influence long-term health is through altered programming of DNA methylation. In this work, we utilized an established mouse model of human-relevant perinatal exposure and enhanced reduced representation bisulfite sequencing to investigate the long-term effects of diethylhexyl phthalate (DEHP) exposure on DNA methylation in the hearts of adult male and female offspring at 5 months of age (n = 5-7 mice per sex and exposure). Perinatal DEHP exposure led to hundreds of sex-specific, differentially methylated cytosines (DMCs) and differentially methylated regions (DMRs) in the heart. Pathway analysis of DMCs revealed enrichment for several pathways in females, including insulin signaling, regulation of histone methylation, and tyrosine phosphatase activity. In males, DMCs were enriched for glucose transport, energy generation, and developmental programs. Notably, many sex-specific genes differentially methylated with DEHP exposure in our mouse model were also differentially methylated in published data of heart tissues collected from human heart failure patients. Together, these data highlight the potential role for DNA methylation in DEHP-induced cardiac effects and emphasize the importance of sex as a biological variable in environmental health studies.
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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.