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Epigenetics: Mechanisms in Toxicology and Disease
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Epigenetics: Mechanisms in Toxicology and Disease

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Epigenomics".

Deadline for manuscript submissions: closed (15 October 2023) | Viewed by 1621

Special Issue Editors

Prof. Dr. Anil Amichund Chuturgoon

E-Mail Website
Guest Editor
Department of Medical Biochemistry, School of Laboratory Medicine and Medical Sciences, College of Health Sciences, University of KwaZulu-Natal, Durban 4041, South Africa
Interests: toxicology; genetics; epigenetics
Special Issues, Collections and Topics in MDPI journals
Dr. Terisha Ghazi

E-Mail Website
Guest Editor
Department of Medical Biochemistry, School of Laboratory Medicine and Medical Sciences, College of Health Sciences, University of KwaZulu-Natal, Durban 4041, South Africa
Interests: toxicology; mycotoxins; epigenetics; DNA methylation; histone modifications; non-coding RNA; epitranscriptomics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We would like to invite you to participate in this Special Issue, “Epigenetics: Mechanisms in Toxicology and Disease”.

Epigenetic mechanisms are reversible modifications that regulate gene expression and, ultimately, cellular function. These modifications, such as DNA methylation, histone modifications, and RNA interference by non-coding RNAs, can be altered by external factors and play a powerful role in toxicological outcomes and human diseases. As a result, emerging evidence has identified changes in epigenetic modifications as biomarkers and targets of therapeutic intervention.

The aim of this Special Issue is to collate original research articles and reviews that explore the current knowledge on epigenetic mechanisms associated with toxicology and human diseases. This includes studies on pharmaceuticals, food contaminants, environmental pollutants, metabolic diseases, and viral diseases, amongst others.

Prof. Dr. Anil Amichund Chuturgoon
Dr. Terisha Ghazi
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Genes is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

 

Keywords

  • epigenetics
  • toxicology
  • DNA methylation
  • histone modifications
  • non-coding RNA
  • food contaminants
  • environmental toxicants
  • human diseases
  • metabolic diseases
  • viral diseases

Published Papers (1 paper)

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Research

13 pages, 1779 KiB  
Article
The Effect of DNA Methylation in the Development and Progression of Chronic Kidney Disease in the General Population: An Epigenome-Wide Association Study Using the Korean Genome and Epidemiology Study Database
by Ji-Eun Kim, Min-Jee Jo, Eunjung Cho, Shin-Young Ahn, Young-Joo Kwon, Jeong-An Gim and Gang-Jee Ko
Genes 2023, 14(7), 1489; https://doi.org/10.3390/genes14071489 - 21 Jul 2023
Cited by 1 | Viewed by 1303
Abstract
Background: Although knowledge of the genetic factors influencing kidney disease is increasing, epigenetic profiles, which are associated with chronic kidney disease (CKD), have not been fully elucidated. We sought to identify the DNA methylation status of CpG sites associated with reduced kidney function [...] Read more.
Background: Although knowledge of the genetic factors influencing kidney disease is increasing, epigenetic profiles, which are associated with chronic kidney disease (CKD), have not been fully elucidated. We sought to identify the DNA methylation status of CpG sites associated with reduced kidney function and examine whether the identified CpG sites are associated with CKD development. Method: We analyzed DNA methylation patterns of 440 participants in the Korean Genome and Epidemiology Study (KoGES) with estimated glomerular filtration rates (eGFRs) ≥ 60 mL/min/1.73 m2 at baseline. CKD development was defined as a decrease in the eGFR of <60 at any time during an 8-year follow-up period (“CKD prediction” analysis). In addition, among the 440 participants, 49 participants who underwent a second methylation profiling were assessed for an association between a decline in kidney function and changes in the degree of methylation of CpG sites during the 8 years (“kidney function slope” analysis). Results: In the CKD prediction analysis, methylation profiles of a total of 403,129 CpG sites were evaluated at baseline in 440 participants, and increased and decreased methylation of 268 and 189 CpG sites, respectively, were significantly correlated with the development of CKD in multivariable logistic regression. During kidney function slope analysis using follow-up methylation profiles of 49 participants, the percent methylation changes in 913 CpG sites showed a linear relationship with the percent change in eGFR during 8 years. During functional enrichment analyses for significant CpG sites found in the CKD prediction and kidney function slope analyses, we found that those CpG sites represented MAPK, PI3K/Akt, and Rap1 pathways. In addition, three CpG sites from three genes, NPHS2, CHCHD4, and AHR, were found to be significant in the CKD prediction analysis and related to a decline in kidney function. Conclusion: It is suggested that DNA methylation on specific genes is associated with the development of CKD and the deterioration of kidney function. Full article
(This article belongs to the Special Issue Epigenetics: Mechanisms in Toxicology and Disease)
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