Epigenetics and Environmental Exposures

A special issue of DNA (ISSN 2673-8856).

Deadline for manuscript submissions: 20 September 2025 | Viewed by 2642

Special Issue Editors


E-Mail Website
Guest Editor
Team Epigenetics, DNA replication and Cancer, Université de Paris, Institut Cochin, INSERM, F-75014 Paris, France
Interests: DNA replication; epigenetics; cancer

E-Mail Website
Guest Editor
School of Agriculture, Food and Wine, Waite Research Institute, University of Adelaide, Adelaide, SA 5005, Australia
Interests: epigenetics; DNA methylation; development

Special Issue Information

Dear Colleagues,

It is well known that our lifestyles, as well as our environment, have a pronounced effect on our organisms. Examples abound of how chemical compounds and xenobiotics present in food, water or the atmosphere are capable of altering epigenetic status and gene expression and thus impact human health. Studies have also shown how diet, anxiety, lack of sleep or a sedentary lifestyle can affect epigenetic status, gene expression and human health. More importantly, some studies have reported on the long-term effects of these exposures or effects linked to low-dose exposure.

Epigenetic modifications (e.g., DNA methylation, histone modifications, histone variants, non-coding RNAs) play a central role in regulating various essential cellular processes. These modifications are extremely sensitive to changes in cell metabolism or cell signalling induced by environmental signals. Characterizing the relationship between environmental exposures, these modifications and their functions is essential to better understand how environmental signals can be linked to disease or long-term effects.

In this Special Issue, we welcome review articles and original research studies exploring these aspects in vitro, in cellular and animal models as well as in human.

Dr. Benoît Miotto
Dr. Tina Bianco-Miotto
Guest Editors

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Keywords

  • epigenetics
  • chemicals
  • histone marks and variants
  • DNA methylation
  • non-coding RNAs
  • diseases
  • chromatin organisation
  • low-dose and cocktail effects

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Published Papers (2 papers)

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Research

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9 pages, 459 KiB  
Article
Child Telomere Length at 11–12 Years of Age Is Not Associated with Pregnancy Complications
by Tina Bianco-Miotto, Sadia Hossain, Nahal Habibi, Dandara G. Haag and Jessica A. Grieger
DNA 2024, 4(2), 180-188; https://doi.org/10.3390/dna4020011 - 11 Jun 2024
Cited by 1 | Viewed by 1199
Abstract
Children born from pregnancy complications are at higher risk of chronic diseases in adulthood. Identifying which children born from a complicated pregnancy are likely to suffer from later chronic disease is important in order to intervene to prevent or delay the onset of [...] Read more.
Children born from pregnancy complications are at higher risk of chronic diseases in adulthood. Identifying which children born from a complicated pregnancy are likely to suffer from later chronic disease is important in order to intervene to prevent or delay the onset of disease. This study examined the associations between the major pregnancy complications (gestational diabetes, high blood pressure, small- and large for gestational age, and preterm birth) and child telomere length, a biomarker of chronic disease risk. This was a population-based longitudinal analysis using data from the Longitudinal Study of Australian Children. The primary outcome is telomere length, measured in 11–12-year-old children. Multivariable linear regression was used to estimate the association between pregnancy complications and child telomere length, adjusting for a range of a priori confounders. Data from 841 families were used. One in four pregnancies (27.1%) featured a pregnancy complication. In the adjusted analysis, there was no association between pregnancy complications and child telomere length (high blood pressure: mean difference (95% CI): 0.00 (−0.12, 0.12); gestational diabetes (0.05 (−0.10, 0.19)); small for gestational age (0.07 (−0.04, 0.19)); large for gestational age (−0.06 (−0.15, 0.03)); and preterm birth (−0.10 (−0.21, 0.01)). Our results do not support the notion that telomere length is shorter in children born to mothers after a pregnancy complication. Methodological considerations should be rigorous to improve the reproducibility of findings. Full article
(This article belongs to the Special Issue Epigenetics and Environmental Exposures)
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Review

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17 pages, 862 KiB  
Review
Chemical Versus Enzymatic Nucleic Acid Modifications and Genomic Stability
by Jonathan R. Cortez and Marie E. Migaud
DNA 2025, 5(2), 19; https://doi.org/10.3390/dna5020019 - 9 Apr 2025
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Abstract
DNA damage and repair have been central themes in cellular biology research. Broadly, DNA damage is understood as modifications to canonical nucleotides that disrupt their function during transcription and replication. A deeper biochemical understanding of DNA damage is essential, as the genome governs [...] Read more.
DNA damage and repair have been central themes in cellular biology research. Broadly, DNA damage is understood as modifications to canonical nucleotides that disrupt their function during transcription and replication. A deeper biochemical understanding of DNA damage is essential, as the genome governs all cellular processes. We can classify DNA damage according to whether the modifications to the nucleic acid scaffold are chemically or enzymatically initiated. This distinction is important because chemical modifications are often irreversible, sometimes sparse, and difficult to detect or control spatially and replicate systematically. This can result in genomic damage or modifications to nucleotides in the nucleotide pool, which is less commonly studied. In contrast, enzymatic modifications are typically induced by the cell for specific purposes and are under strong regulatory control. Enzymatic DNA modifications also present a degree of sequence specificity and are often reversible. However, both types of DNA modifications contribute to cellular aging when poorly repaired and, as a result, remain incompletely understood. This review hopes to gather less studied mechanisms in nucleotide modifications and show research gaps in our current understanding of nucleotide biology. By examining the implications of these mechanisms on DNA modifications, in the nucleotide pool and genome, we may gain insights into innovative strategies for mitigating the effects of cellular aging. Full article
(This article belongs to the Special Issue Epigenetics and Environmental Exposures)
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