ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Deciphering the mechanism of aristolochic acid I-driven hepatocellular carcinoma through integrated network toxicology and bioinformatics.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Harnessing the neuroprotective potential of estrogen in Parkinson's disease: an insight into molecular mechanisms and therapeutic approaches.Metabolic brain disease · 2026Review
- Unveiling the Immunopharmacological Mechanisms of Biejiajian Pills (BJJP) Underlying the Treatment of Hepatic Fibrosis: Insights From Network Pharmacology and Experimental Validation.Food science & nutrition · 2026Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Aristolochic acid I (AAI) is a known liver carcinogen, but its molecular mechanisms in hepatocellular carcinoma (HCC) remain incompletely understood. This study aimed to systematically elucidate these mechanisms. This study employed a multidisciplinary strategy: assessing AAI carcinogenicity via ProTox-3.0; identifying its targets using PubChem; and screening HCC-related genes from GEO. Core genes were filtered through network toxicology and Lasso-Cox regression. Molecular docking and dynamics simulations analyzed AAI-protein interactions, while GO, KEGG, and GSEA enrichment revealed relevant pathways. Key gene expression and clinical relevance were validated via TCGA and HPA databases. The carcinogenic potential of the AAI was 0.77. Fifty-two potential targets of AAI-induced HCC were identified. Network toxicology analysis identified 12 core genes including EZH2, FABP5, and RXRA. Lasso-Cox regression analysis identified four core genes that drive HCC progression, including EZH2. Functional enrichment analysis revealed that AAI-HCC targets were significantly enriched in lipid metabolism and the PPAR signaling pathway (p < 0.05), with the PPAR signaling pathway being significantly activated in HCC. Molecular docking and MD simulations confirmed the high affinity and stable binding of AAI to EZH2, FABP5, and RXRA. Through in silico and database-based validation, biological samples and clinical data confirmed that these genes were significantly overexpressed in HCC (p < 0.001) and were correlated with poor prognosis (p < 0.01). AAI may synergistically activate the PPAR signaling pathway by targeting EZH2, FABP5, and RXRA, driving lipid metabolism reprogramming and promoting the occurrence and development of HCC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.