Integration of Animal Models and Omics Technologies for Exploring Toxicity Mechanisms

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Novel Methods in Toxicology Research".

Deadline for manuscript submissions: 30 September 2026 | Viewed by 230

Special Issue Editor

School of Life Sciences, Jiangsu University, Zhenjiang 212013, China
Interests: toxicity; animal models; proteomics; metabolomics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Toxics is pleased to announce this Special Issue, which will focus on advancing our mechanistic understanding of toxic outcomes through innovative experimental designs and integrative analytical frameworks. We invite submissions that employ diverse animal models—spanning vertebrates, invertebrates, and alternative model systems—to elucidate tissue‑specific, developmental, or systemic toxicity. Special emphasis will be placed on studies that combine high‑throughput multi‑omics technologies (e.g., transcriptomics, proteomics, metabolomics) with classical toxicological endpoints to uncover novel mechanistic pathways and robust biomarker signatures.

We welcome original research and reviews on the following topics:

  • Cutting‑edge in vivo or ex vivo models to dissect toxicity mechanisms beyond apical observations;
  • Applications of integrative omics to identify predictive biomarker panels for early detection or mechanistic classification;
  • Cross‑species comparisons to enhance translational relevance.

This Special Issue aims to showcase interdisciplinary studies that bridge molecular phenotyping with functional toxicity assessment, fostering the development of more predictive and mechanism‑based safety evaluation paradigms.

Dr. Liang Chen
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. Toxics 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

  • toxicity
  • animal models
  • biomarker
  • multi‑omics
  • mechanistic toxicology

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Published Papers (1 paper)

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Research

21 pages, 4038 KB  
Article
Combined Analysis of Network Toxicology and Metabolomics Uncovers the Potential Mechanisms Underlying Neodymium Oxide-Induced Pulmonary Fibrosis
by Kai Wu, Yi Zhang, Xi Chen, Yanhong Dong, Suhua Wang and Yanrong Gao
Toxics 2026, 14(6), 513; https://doi.org/10.3390/toxics14060513 - 12 Jun 2026
Viewed by 1
Abstract
Rare earth element-related occupational and environmental health risks have received increasing attention, but the molecular mechanisms underlying neodymium oxide (Nd2O3)-induced pulmonary fibrosis remain unclear. This study aimed to identify potential targets, metabolites, and pathways involved in fibrosis-related lung responses [...] Read more.
Rare earth element-related occupational and environmental health risks have received increasing attention, but the molecular mechanisms underlying neodymium oxide (Nd2O3)-induced pulmonary fibrosis remain unclear. This study aimed to identify potential targets, metabolites, and pathways involved in fibrosis-related lung responses after Nd2O3 exposure. An integrated network toxicology and metabolomics approach was combined with an in vivo mouse model of Nd2O3-induced pulmonary toxicity. Histopathological injury, collagen deposition, and fibrosis-related protein expression were evaluated by HE staining, Masson staining, and Western blotting, respectively. Candidate targets were identified from public databases, key pathways were analyzed through network construction, and selected genes were validated by RT-qPCR. Nd2O3 exposure caused evident lung injury, inflammatory cell infiltration, structural disruption, increased collagen deposition, and elevated fibrosis-related protein expression. A total of 162 overlapping targets related to Nd2O3 exposure and pulmonary fibrosis were identified. ESR1, PTGS2, HSP90AA1, and MMP9 emerged as key targets, while cAMP signaling, arachidonic acid metabolism, PI3K-Akt signaling, and efferocytosis-related processes were implicated. Metabolomics showed distinct separation between control and high-exposure groups, with differential metabolites mainly associated with lipid metabolism and inflammation. RT-qPCR further confirmed altered expression of key genes. These findings suggest that Nd2O3 may promote fibrosis-related lung responses through inflammatory signaling, lipid metabolic disturbance, and profibrotic pathway activation. Full article
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