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Epigenetics in Molecular Toxicology
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Epigenetics in Molecular Toxicology

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 5065

Special Issue Editor

Dr. Maricica Pacurari

E-Mail Website
Guest Editor
Department of Biology, College of Science, Engineering, and Technology, Jackson State University, Jackson, MS 39217, USA
Interests: lung cancer; lung fibrosis; nanotoxicogenomics; endothelial dysfunction; molecular network interactions
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We invite you to This Special Issue to bring forward epigenetics mechanisms that contribute to organ dysfunction, organ rejection, disease development, or immunosuppression. Therefore, this Special Issue is dedicated to understanding how epigenetics such as DNA methylation, histone modifications, non-coding RNAs are regulated and how their perturbed mechanisms play a key role in gene expression and disease development. This being said, in this Special Issue, we invite the scientific community to address what might regulate epigenetics, the mechanisms how epigenetics influence signaling pathways in organ injury, organ rejection, cancer, fibrosis, cardiovascular disease, diabetes, and immunosuppression. We invite original research articles and reviews on the future of epigenetics in translational medicine for a peer-review and publication in this Special Issue of Epigenetics in Molecular Toxicology. We are excited to address such an intricate topic yet with profound biological effects.

Dr. Maricica Pacurari
Guest Editor

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • DNA methylation
  • histones modifications
  • long noncoding RNA
  • microRNA
  • signal transduction
  • regulation
  • hormones
  • disease
  • development
  • inflammation
  • oxidative stress
  • cytokines
  • organ injury
  • cancer
  • diabetes
  • fibrosis
  • acute response
  • chronic response
  • environmental

Published Papers (2 papers)

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Research

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11 pages, 2483 KiB  
Article
Role of Glycolysis/Gluconeogenesis and HIF-1 Signaling Pathways in Rats with Dental Fluorosis Integrated Proteomics and Metabolomics Analysis
by Yue Ba, Shuo Yang, Shuiyuan Yu, Xiangbo Hou, Yuhui Du, Minghui Gao, Juan Zuo, Lei Sun, Xiaoli Fu, Zhiyuan Li, Hui Huang, Guoyu Zhou and Fangfang Yu
Int. J. Mol. Sci. 2022, 23(15), 8266; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23158266 - 27 Jul 2022
Cited by 3 | Viewed by 1946
Abstract
Fluoride is widely distributed, and excessive intake will lead to dental fluorosis. In this study, six offspring rats administrated 100 mg/L sodium fluoride were defined as the dental fluorosis group, and eight offspring rats who received pure water were defined as the control [...] Read more.
Fluoride is widely distributed, and excessive intake will lead to dental fluorosis. In this study, six offspring rats administrated 100 mg/L sodium fluoride were defined as the dental fluorosis group, and eight offspring rats who received pure water were defined as the control group. Differentially expressed proteins and metabolites extracted from peripheral blood were identified using the liquid chromatography tandem mass spectrometry and gas chromatography mass spectrometry, with the judgment criteria of fold change >1.2 or <0.83 and p < 0.05. A coexpression enrichment analysis using OmicsBean was conducted on the identified proteins and metabolites, and a false discovery rate (FDR) < 0.05 was considered significant. Human Protein Atlas was used to determine the subcellular distribution of hub proteins. The Gene Cards was used to verify results. A total of 123 up-regulated and 46 down-regulated proteins, and 12 up-regulated and 2 down-regulated metabolites were identified. The significant coexpression pathways were the HIF-1 (FDR = 1.86 × 10−3) and glycolysis/gluconeogenesis (FDR = 1.14 × 10−10). The results of validation analysis showed the proteins related to fluorine were mainly enriched in the cytoplasm and extrinsic component of the cytoplasmic side of the plasma membrane. The HIF-1 pathway (FDR = 1.01 × 10−7) was also identified. Therefore, the HIF-1 and glycolysis/gluconeogenesis pathways were significantly correlated with dental fluorosis. Full article
(This article belongs to the Special Issue Epigenetics in Molecular Toxicology)
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Review

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18 pages, 1004 KiB  
Review
THE MAIN CYTOTOXIC EFFECTS OF METHYLSELENINIC ACID ON VARIOUS CANCER CELLS
by Elena G. Varlamova and Egor A. Turovsky
Int. J. Mol. Sci. 2021, 22(12), 6614; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22126614 - 21 Jun 2021
Cited by 32 | Viewed by 2583
Abstract
Studies of recent decades have repeatedly demonstrated the cytotoxic effect of selenium-containing compounds on cancer cells of various origins. Particular attention in these studies is paid to methylseleninic acid, a widespread selenium-containing compound of organic nature, for several reasons: it has a selective [...] Read more.
Studies of recent decades have repeatedly demonstrated the cytotoxic effect of selenium-containing compounds on cancer cells of various origins. Particular attention in these studies is paid to methylseleninic acid, a widespread selenium-containing compound of organic nature, for several reasons: it has a selective cytotoxic effect on cancer cells, it is cytotoxic in small doses, it is able to generate methylselenol, excluding the action of the enzyme β-lyase. All these qualities make methylseleninic acid an attractive substrate for the production of anticancer drugs on its basis with a well-pronounced selective effect. However, the studies available to date indicate that there is no strictly specific molecular mechanism of its cytotoxic effect in relation to different cancer cell lines and cancer models. This review contains generalized information on the dose- and time-dependent regulation of the toxic effect of methylseleninic acid on the proliferative properties of a number of cancer cell lines. In addition, special attention in this review is paid to the influence of this selenium-containing compound on the regulation of endoplasmic reticulum stress and on the expression of seven selenoproteins, which are localized in the endoplasmic reticulum. Full article
(This article belongs to the Special Issue Epigenetics in Molecular Toxicology)
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