ArticleMetabolomics : Official journal of the Metabolomic Society2024
Study on the molecular mechanism of atopic dermatitis in mice based on skin and serum metabolomic analysis.
Article in Metabolomics : Official journal of the Metabolomic Society, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Beyond the Skin: Exploring the Gut-Skin Axis and Metabolic Pathways in Atopic Dermatitis Pathogenesis.International journal of general medicine · 2025Review
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Authors and funding
5 authors.
Funding
Abstract
introductionAtopic dermatitis (AD) is a common chronic inflammatory dermatosis. However, the exact molecular mechanism underlying the development of AD remain largely unclear.
objectiveTo investigate comprehensive metabolomic alterations in serum and skin tissue between 2,4-dinitrofluorobenzene (DNFB)-induced AD-like mice and healthy controls, aiming to identify the potential disease biomarkers and explore the molecular mechanisms of AD.
methodsIn this study, Untargeted metabolomics analysis was used to investigate both skin and serum metabolic abnormalities of 2,4-dinitrofluorobenzene (DNFB)-induced AD-like mice. Then, the metabolic differences among the groups were determined through the application of multivariate analysis. Additionally, the selection of predictive biomarkers was accomplished using the receiver operating characteristic (ROC) module.
resultsOur findings showed that levels of 220 metabolites in the skin and 94 metabolites in the serum were different in AD-like mice that were treated with DNFB compared to control mice. Uracil, N-Acetyl-L-methionine, deoxyadenosine monophoosphate, 2-acetyl-l-alkyl-sn-glycero-3-phosphcholine, and prostaglandin D2 are considered potential biomarkers of AD as obtained by integrating skin and serum differential metabolite results. Metabolomic data analysis showed that the metabolic pathways in which skin and serum are involved together include histidine metabolism, pyrimidine metabolism, alanine, aspartate, and glutamate metabolism.
conclusionOur research explained the possible molecular mechanism of AD at the metabolite level and provided potential targets for the development of clinical drugs for AD.
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