ArticleJournal of translational internal medicine2026
Application of metabolomics in drug-induced liver injury: A systematic review.
Article in Journal of translational internal medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Drug-induced liver injury (DILI) is one of the most common adverse reactions in clinical settings, and drug hepatotoxicity is also a primary factor contributing to the suspension and withdrawal of drug development. Currently, there are no specific biomarkers available for the early diagnosis and monitoring of DILI in clinical practice. In recent years, metabolomics has emerged as a powerful tool for identifying small molecule biomarkers in DILI, owing to its unique advantages. In this article, we comprehensively reviewed the metabolomics studies related to DILI to investigate the pathophysiological changes in DILI and to assess the potential application of metabolomics in its prediction and diagnosis. Relevant literature published before 30 April 2024 was retrieved from four online databases (PubMed, EMbase, Cochrane Library, and Web of Science). Research data were systematically collected, and the metabolites involved were analyzed. Metabolic pathway analysis related to DILI was conducted using the online software MetaboAnalyst 5.0. A total of 55 studies were included, identifying significantly altered metabolic pathways and valuable metabolic biomarkers. The most frequently reported biomarkers included glycocholic acid, taurochenodeoxycholic acid, taurocholic acid, creatine, glycochenodeoxycholic acid, taurodeoxycholic acid, glycodeoxycholic acid, and
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