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25th Anniversary of IJMS: Updates and Advances 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: 30 January 2026 | Viewed by 328

Special Issue Editor

Dr. Marco E. M. Peluso

E-Mail Website
Guest Editor
Cancer Risk Factor Branch, Regional Cancer Prevention Laboratory, Study, Prevention and Oncology Network Institute (ISPRO), 50139 Florence, Italy
Interests: genetic damage; oxidative stress; DNA adducts; epigenetics; mutations; carcinogenesis; molecular epidemiology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

By identifying biomarkers of exposure and effect, molecular toxicology can elucidate the mechanisms of toxicity of environmental agents and inform risk assessment and policy decisions, focusing on the risks posed to human health. Improved understanding can allow for more precise diagnosis, personalized treatment strategies, and a better knowledge of how environmental agents contribute to the development of human diseases. Therefore, this Special Issue, 25th Anniversary of IJMS: Updates and Advances in Molecular Toxicology, aims to collect original research contributions on the most recent investigations in this field that can help to delucidate the interactions between chemical molecules and organisms by providing tools to understand chronic diseases, including cancer, at its fundamental molecular level. Topics of interest include, but are not limited to, the study of defined xenobiotics compounds such as cancerogenic agents, metals, endocrine and epigenetic disruptors, and the association between exposure to toxic substances and the diagnosis of human diseases by using in vivo and in vitro models, as well as case–control and cross-sectional approaches. We hope that this Special Issue will prompt advances in molecular toxicology as well its application in cancer diagnostics.

Dr. Marco E. M. Peluso
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 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-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.

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Keywords

  • molecular toxicology
  • biomarkers
  • mechanisms of toxicity
  • xenobiotics
  • cancer diagnosis

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Published Papers (2 papers)

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Research

28 pages, 10855 KB  
Article
Molecular Mechanisms of Aspartame-Induced Kidney Renal Papillary Cell Carcinoma Revealed by Network Toxicology and Molecular Docking Techniques
by Chenjie Huang, Lulu Wei, Wenqi Yuan, Yaohong Lu, Gedi Zhang and Ziyou Yan
Int. J. Mol. Sci. 2026, 27(1), 77; https://doi.org/10.3390/ijms27010077 (registering DOI) - 21 Dec 2025
Abstract
Aspartame, a widely used artificial sweetener, has been linked to various cancers, including kidney renal papillary cell carcinoma (KIRP). However, the molecular mechanisms underlying this association remain unclear. This study employed network toxicology and molecular docking to investigate potential mechanisms of aspartame-induced KIRP. [...] Read more.
Aspartame, a widely used artificial sweetener, has been linked to various cancers, including kidney renal papillary cell carcinoma (KIRP). However, the molecular mechanisms underlying this association remain unclear. This study employed network toxicology and molecular docking to investigate potential mechanisms of aspartame-induced KIRP. Differentially expressed genes from TCGA were intersected with aspartame targets and KIRP-related genes, yielding 61 common targets. GO and KEGG analyses revealed enrichment in extracellular matrix degradation, signaling pathways, and immune microenvironment regulation. Univariate Cox regression identified 23 prognostically significant genes, from which multifactorial Cox regression with stepwise selection determined 8 core genes (APLNR, CYP2C19, EDNRA, KLK5, F2R, RAD51, AURKA, and TLR2). A risk model was constructed and validated through VIF analysis, Schoenfeld residual testing, and internal validation using a training–validation split. SHAP analysis identified EDNRA as the primary driver gene. Survival analysis demonstrated that the model effectively stratified KIRP patients, with risk score and tumor stage serving as independent prognostic factors. Molecular docking confirmed stable binding between aspartame and core target proteins. These findings provide mechanistic insights into aspartame-induced KIRP pathogenesis and establish a foundation for future experimental validation. Full article
(This article belongs to the Special Issue 25th Anniversary of IJMS: Updates and Advances in Molecular Toxicology)
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18 pages, 5040 KB  
Article
B-Cell Receptor-Associated Protein 31 Deficiency Aggravates Ethanol-Induced Liver Steatosis and Liver Injury via Attenuating Fatty Acid Oxidation and Glycogen Synthesis
by Shubin Yu, Yaodong Xia, Chunyan Zhang, Xiangyue Han, Xiaoyue Feng, Liya Li, Hang Ma and Jialin Xu
Int. J. Mol. Sci. 2025, 26(24), 12173; https://doi.org/10.3390/ijms262412173 - 18 Dec 2025
Viewed by 166
Abstract
Alcoholic liver disease (ALD) is a spectrum of alcohol-induced disorders and represents a major global health challenge. B-cell receptor-associated protein 31 (BAP31) is an endoplasmic reticulum-resident chaperone involved in protein transport, apoptosis, cancer biology, and lipid metabolism. To explore its role in ALD, [...] Read more.
Alcoholic liver disease (ALD) is a spectrum of alcohol-induced disorders and represents a major global health challenge. B-cell receptor-associated protein 31 (BAP31) is an endoplasmic reticulum-resident chaperone involved in protein transport, apoptosis, cancer biology, and lipid metabolism. To explore its role in ALD, we used hepatocyte-specific BAP31 knockout mice (BAP31-LKO) and wild-type (WT) littermates exposed to ethanol to assess BAP31′s biochemical and metabolic impact. Following ethanol exposure, BAP31-LKO mice exhibited elevated serum alanine transaminase (23.2%, p < 0.05) and aspartate transaminase (31.4%, p < 0.05) levels compared to WT mice. Increased malondialdehyde (8.5%, p < 0.05) and reduced superoxide dismutase (22.8%, p < 0.05) in BAP31-LKO mice indicate exacerbated liver injury. Furthermore, BAP31 deficiency increased triglyceride (35.7%, p < 0.05) and free fatty acid (16.2%, p < 0.05) accumulation following ethanol treatment, while the expression of fatty acid oxidation-related genes, including Pparα, Cd36, Fatp2, Cpt2, and Acox1, was reduced in BAP31-LKO mice. The mRNA levels of Xbp1, Xbp1s, and Chop, as well as protein levels of p-eIF2α, IRE1α, GRP78, and CHOP, were increased in BAP31-LKO mice compared to WT controls, indicating aggravated ethanol-induced ER stress. Hepatic glycogen content was also reduced in BAP31-LKO mice, along with reduced Ppp1r3c expression, demonstrating impaired glycogen synthesis. Consistently, BAP31 knockdown amplified ethanol-induced lipid accumulation, inflammation, impaired glycogen storage, ER stress, and suppression of Pparα signaling in HepG2 cells. Together, these findings demonstrate that BAP31 deficiency exacerbates ethanol-induced liver steatosis, inflammation, and liver injury by impairing fatty acid oxidation and glycogen synthesis, and by amplifying ER stress responses. Full article
(This article belongs to the Special Issue 25th Anniversary of IJMS: Updates and Advances in Molecular Toxicology)
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