Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
5.9
3.1
Journals
Genes
Special Issues
Environmental Genomics and Low-Dose Induced Adaptive Response: Underlying Mechanisms from...
share announcement

Environmental Genomics and Low-Dose Induced Adaptive Response: Underlying Mechanisms from Cells to Organisms

A Special Issue of Genes (ISSN 2073-4425) belonging to the section "Genes & Environments".

Deadline for manuscript submissions: 20 March 2027 | Viewed by 4069

Editors

Prof. Dr. Stephka Chankova

E-Mail Website
Guest Editor
Institute of Biodiversity and Ecosystem Research, Bulgarian Academy of Sciences, Sofia, Bulgaria
Interests: low-dose adaptive response (AR); the contribution of DNA repair; antioxidant and chaperone systems for the formation of an AR; genotypes and induced resistance; screening of genotoxics; mutagenic effects of environmental pollutants; lower eukaryotes; higher plants; anti-mutagenesis
Prof. Dr. Michaela Beltcheva

E-Mail Website
Guest Editor
Institute of Biodiversity and Ecosystem Research, Bulgarian Academy of Sciences, Sofia, Bulgaria
Interests: small mammals; eco-toxicology; eco-physiology; adaptive responses at different levels of biological organization to various environmental pollutants
Dr. Teodora Todorova

E-Mail Website
Guest Editor
Institute of Biodiversity and Ecosystem Research, Bulgarian Academy of Sciences, 1113 Sofia, Bulgaria
Interests: mutagenesis/antimutagenesis; anticarcinogenesis; oxidative stress; natural products; low-dose adaptive response; mechanisms of DSBs induction and repair; Ty1 retrotransposition; genome stability
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to announce the launch of the Special Issue "Environmental Genomics and Low-Dose Induced Adaptive Response: Underlying Mechanisms from Cells to Organisms". This Special Issue calls for original research and reviews that explore the genomic and molecular foundations of adaptive responses triggered by low-dose exposure to environmental stressors, including radiation and genotoxic chemicals. The central focus is on the phenomenon of induced resistance (the adaptive response), a critical radio-protective mechanism formally recognized by the International Atomic Energy Agency and the World Health Organization for its implications in human and environmental health. We welcome contributions that use cutting-edge environmental genomics, mutagenesis screening, epigenomics, and molecular techniques to decipher the signaling pathways that enable this protection—from activation of DNA repair, as well as antioxidant and chaperone defenses, to systemic organismal resilience. At higher levels of biological organization, the submission of eco-toxicological research is encouraged, particularly research focused on how low-dose environmental stressors shape whole organisms’ physiology, fitness, and adaptive resilience in natural or experimental populations. This collection aims to synthesize knowledge about the dual aspects of environmental mutagenesis and the low-dose induced adaptive response, ultimately improving our understanding of the mechanisms of biological defense and informing environmental risk assessment and public health strategies.

Prof. Dr. Stephka Chankova
Prof. Dr. Michaela Beltcheva
Dr. Teodora Todorova
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 250 words) can be sent to the Editorial Office for assessment.

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-anonymized 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

  • environmental genomics
  • ecotoxicology
  • low-dose induced adaptive response
  • low-dose radiation
  • genomic instability
  • environmental mutagenesis
  • DNA repair
  • radio-protection
  • stress response
  • toxicogenomics
  • antioxidant system
  • chaperone system

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (4 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

18 pages, 22102 KB  
Article
Genetic Susceptibility to Impaired Lung Function in Underground Coal Miners from Kazakhstan
by Anastassiya Perfilyeva, Sayagul Kairgeldina, Alexandr Gulyayev, Kanat Tekebayev, Kanagat Yergali, Ozada Khamdiyeva, Sholpan Koigel’dinova, Zhanbol Sabirov, Nazym Sagandykova, Madina Baurzhan and Gulnur Zhunussova
Genes 2026, 17(9), 1021; https://doi.org/10.3390/genes17091021 - 27 Aug 2026
Viewed by 315
Abstract
Background/Objectives: Occupational exposure to coal mine dust is a major risk factor for respiratory impairment; however, the genetic determinants of individual variation in lung function remain poorly understood, particularly in occupational cohorts that have been largely absent from genome-wide association studies. This study [...] Read more.
Background/Objectives: Occupational exposure to coal mine dust is a major risk factor for respiratory impairment; however, the genetic determinants of individual variation in lung function remain poorly understood, particularly in occupational cohorts that have been largely absent from genome-wide association studies. This study aimed to identify genetic variants associated with quantitative lung function traits in underground coal miners from Kazakhstan. Methods: A total of 186 underground coal miners from the Karaganda coal basin were genotyped using the Illumina Global Screening Array. Genome-wide association analyses were performed for six spirometric parameters (FVC, FEV1, FEV1/FVC, MEF25, MEF50, and MEF75), adjusting for age, mining exposure, body mass index, smoking status, and population structure. Genotype imputation was performed to increase genomic coverage and evaluate the consistency of association signals. Results: No variants reached the conventional genome-wide significance threshold. However, recurrent suggestive associations identified PRKCB, FANCE, and UBTD1 as the principal candidate loci across correlated spirometric parameters, with independent support from genotype imputation. Conclusions: Recurrent associations across complementary spirometric parameters identified biologically plausible candidate loci involved in inflammatory signalling, DNA repair, and epithelial homeostasis. These findings provide one of the first genomic insights into lung function in underground coal miners and provide a foundation for future validation and functional studies. Full article
(This article belongs to the Special Issue Environmental Genomics and Low-Dose Induced Adaptive Response: Underlying Mechanisms from Cells to Organisms)
►▼ Show Figures

Figure 1

15 pages, 1099 KB  
Article
Prenatal Substance Exposure Is Associated with Increased Placental DRD1 Dopamine Receptor Gene Expression and Striatal Gray Matter Volume in Children
by Tara E. Samson, Donato DeIngeniis, Maki S. Koyama, Roberto Bailey, Claire J. Brabander, Ariadna Cilleros Portet, Corina Lesseur, Ahmed Duke Shereen and Yoko Nomura
Genes 2026, 17(8), 958; https://doi.org/10.3390/genes17080958 - 15 Aug 2026
Viewed by 462
Abstract
Background/Objectives: Prenatal substance exposure (PSE) to alcohol, cannabis, and other psychoactive drugs affects over 500,000 pregnancies annually in the US and is consistently associated with adverse birth and childhood outcomes, but the underlying biological mechanisms are not well-understood. Given the dopaminergic system’s role [...] Read more.
Background/Objectives: Prenatal substance exposure (PSE) to alcohol, cannabis, and other psychoactive drugs affects over 500,000 pregnancies annually in the US and is consistently associated with adverse birth and childhood outcomes, but the underlying biological mechanisms are not well-understood. Given the dopaminergic system’s role in substance use and child development, this study aimed to examine and connect the effects of PSE on dopaminergic placental gene expression at birth and on striatal brain volumes in middle childhood. We hypothesized that PSE would lead to reduced dopamine receptor D1 (DRD1) gene expression and smaller striatal gray-matter volumes (GMVs) and that placental DRD1 gene expression would be positively associated with striatal GMV. Methods: PSE, placental gene expression, and T1-weighted MRI data were drawn from a pilot study (n = 34) within the longitudinal cohort Stress in Pregnancy study. PSE was defined by any amount of alcohol, tobacco, or cannabis use during pregnancy. Results: Unexpectedly, children with PSE had a trend toward increased placental DRD1 gene expression (β = 0.497, p = 0.056) and significantly larger GMV in the right putamen (β = 0.374, p = 0.018) and nucleus accumbens (NAc) (β = 0.389, p = 0.029) than unexposed children. Independent of PSE, higher placental DRD1 gene expression at birth was also associated with larger right NAc GMV (β = 0.617, p = 0.015) in middle childhood. Conclusions: These findings contrast prior cross-sectional work linking high-dosage PSE to smaller striatal volumes and inconsistent patterns of dopaminergic gene expression, suggesting potential compensatory placental mechanisms reflected in biological outcomes across child development. Full article
(This article belongs to the Special Issue Environmental Genomics and Low-Dose Induced Adaptive Response: Underlying Mechanisms from Cells to Organisms)
►▼ Show Figures

Graphical abstract

24 pages, 31127 KB  
Article
Integrative Network Toxicology Reveals Potential Molecular Targets Linking Plasticizer Exposure to Inflammatory Gastrointestinal Disorders
by Yongqi Chen, Jiyuan Shi, Yun Ruan, Jinghan Guan, Miaohan Yan, Zongying Zhang, Luojin Wu, Mengmeng Sang, Xinfeng Wang, Liming Mao and Zhaoxiu Liu
Genes 2026, 17(6), 667; https://doi.org/10.3390/genes17060667 - 7 Jun 2026
Viewed by 801
Abstract
Background: Plasticizers, including phthalate esters and phthalate-free alternatives, are widely detected environmental chemicals. Although increasing evidence suggests that plasticizers may disrupt gastrointestinal homeostasis, their potential molecular links with inflammatory gastrointestinal disorders (IGDs) remain unclear. Methods: This study aimed to systematically identify potential molecular [...] Read more.
Background: Plasticizers, including phthalate esters and phthalate-free alternatives, are widely detected environmental chemicals. Although increasing evidence suggests that plasticizers may disrupt gastrointestinal homeostasis, their potential molecular links with inflammatory gastrointestinal disorders (IGDs) remain unclear. Methods: This study aimed to systematically identify potential molecular targets and pathways linking representative plasticizers with IGDs. An integrative network toxicology framework was applied to investigate four plasticizers, including dimethyl phthalate (DMP), diethyl phthalate (DEP), dioctyl phthalate/di(2-ethylhexyl) phthalate (DOP/DEHP), and acetyl tributyl citrate (ATBC), in relation to Crohn’s disease (CD), ulcerative colitis (UC), esophagitis, and gastritis. Plasticizer- and disease-related targets were collected from public databases, followed by overlapping target screening, protein–protein interaction network analysis, functional enrichment analysis, GEO-based transcriptomic validation, molecular docking, molecular dynamics simulation, and single-cell RNA-seq analysis. Results: Disease-specific candidate targets were identified, including CXCL8 and FN1 for CD, IL1B for UC, MAPK3, FASN, FN1, PPARG, CXCL8, FOS, and HIF1A for esophagitis, and MMP9, TNF, TLR4, IL6, CCR2, IFNG, and PTGS2 for gastritis. Cross-disease analysis further identified plasticizer-associated signature targets, including MMP7 for DMP, HMOX1 and NOS2 for DEP, and LTF and CCL11 for ATBC. Enrichment analysis indicated that these targets were mainly involved in inflammatory, chemokine, MAPK-related, and xenobiotic response pathways. Molecular docking and dynamics simulations suggested stable interactions between selected plasticizers and candidate targets, while single-cell analysis revealed their cell-type-specific expression patterns in epithelial, immune, and stromal compartments. Conclusions: This study provides an exploratory network toxicology framework for identifying potential molecular associations between plasticizer exposure and IGDs. The findings highlight disease-specific and plasticizer-associated candidate targets that may guide future experimental validation and environmental risk assessment. Full article
(This article belongs to the Special Issue Environmental Genomics and Low-Dose Induced Adaptive Response: Underlying Mechanisms from Cells to Organisms)
►▼ Show Figures

Figure 1

20 pages, 2441 KB  
Article
Identification of Radiation-Induced Injury Pathways and Hub Genes from RNA-Seq Data Based on Integrative Bioinformatics Approach
by Khalish Arsy Al Khairy Siregar, Chi-Ho Lee, Jong-Jin Kim, Dong-Jo Chang and Seung-Hyun Jeong
Genes 2026, 17(4), 377; https://doi.org/10.3390/genes17040377 - 27 Mar 2026
Viewed by 1820
Abstract
Background: Ionizing radiation (IR) induces profound bone marrow (BM) injury by disrupting hematopoietic stem cell (HSC) homeostasis, leading to acute myelosuppression and long-term hematopoietic dysfunction. Although transcriptome-wide analyses have advanced our understanding of radiation responses, the key molecular networks and hub genes governing [...] Read more.
Background: Ionizing radiation (IR) induces profound bone marrow (BM) injury by disrupting hematopoietic stem cell (HSC) homeostasis, leading to acute myelosuppression and long-term hematopoietic dysfunction. Although transcriptome-wide analyses have advanced our understanding of radiation responses, the key molecular networks and hub genes governing post-irradiation BM injury remain incompletely defined. Methods: This study aimed to systematically identify radiation-responsive pathways and central genes in BM after irradiation through an integrative bioinformatics approach based on RNA sequencing (RNA-seq). Public RNA-seq data from mouse BM HSCs collected 3 days after whole-body irradiation were analyzed. Differentially expressed genes (DEGs) were identified using two independent statistical frameworks to improve the robustness of the results. Functional analysis was performed through Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA). Protein–protein interaction (PPI) networks were constructed using STRING, and hub genes were identified using network topology parameters. Results: Both analysis pathways consistently demonstrated extensive transcriptome reprogramming after irradiation. DEGs were primarily enriched in processes related to cytokine signaling, hematopoietic lineage regulation, immune response, and extracellular matrix remodeling. KEGG analysis highlighted cytokine–cytokine receptor interaction, hematopoietic cell lineage, JAK-STAT signaling, and PI3K-Akt signaling as key molecular axes. GSEA further supported coordinated changes in pathways related to inflammatory response, stress response, and metabolic reprogramming. PPI network analysis identified four consensus hub genes, namely Il6, Cd34, Gypa, and Pdgfrb, which are related to inflammatory signaling, hematopoietic regulation, erythroid dynamics, and microenvironmental remodeling, respectively. Conclusion: This integrative bioinformatics study demonstrates that radiation-induced BM injury is associated with coordinated activation of inflammatory cytokine networks, alterations in the hematopoietic program, and microenvironmental restructuring. The hub genes identified in this study may represent candidate regulatory genes or molecular indicators potentially involved in the response to radiation-induced hematopoietic damage. Full article
(This article belongs to the Special Issue Environmental Genomics and Low-Dose Induced Adaptive Response: Underlying Mechanisms from Cells to Organisms)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-4
Back to TopTop