ArticleFrontiers in medicine2025
Genetic insights into alcohol-associated liver disease: integrative transcriptome-wide analysis identifies novel susceptibility genes.
Article in Frontiers in medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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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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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Preclinical Analysis of Bone Marrow-Derived Stem Cell Therapy Response and Transcriptomic Overlap Analysis in a Severe Alcoholic Hepatitis Mouse Model.Gut and liver · 2026Pooled it
- Genetic and genomic insights across the steatotic liver disease spectrum.Clinical and molecular hepatology · 2026Review
- Shared Genetic Architecture and Multidimensional Modifiable Correlates between Myopia and Retinal-Optic Nerve Diseases.Ophthalmology science · 2026Article
- Genetics and epigenetics in tumor necrosis factor-alpha (Frontiers in medicine · 2026Article
- Gut microbiome in alcohol-associated liver disease: interactions and therapeutic strategies.Frontiers in pharmacology · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Alcohol-associated liver disease (ALD) is a chronic condition influenced by both genetic and environmental factors. While GWAS has identified ALD-related loci (PNPLA3, MBOAT7, TM6SF2), underlying genetic mechanisms and therapeutic targets remain unclear. Methods: This study utilized the FinnGen R12 dataset (488,982 participants) and GTEx v8 eQTL data to perform a cross-tissue transcriptome-wide association study (TWAS) using UTMOST, with single-tissue validation via FUSION. Gene-level association analysis (MAGMA), Mendelian randomization (MR), and colocalization were applied to evaluate causal links. Functional significance was assessed through GeneMANIA, drug enrichment, and molecular docking analyses. Results: Three ALD susceptibility genes-AFF1, C4orf36, and HSD17B13-were identified and validated. HSD17B13 may reduce ALD risk via lipid metabolism and redox balance, while AFF1 is implicated in transcription regulation. C4orf36 requires further study. Drug enrichment analysis highlighted AFF1 as a target for beta-D-allopyranose, dexbrompheniramine, and (+)-chelidonine, with molecular docking confirming strong binding potential. Conclusion: This study identifies AFF1, C4orf36, and HSD17B13 as ALD susceptibility genes, proposing AFF1 as a potential therapeutic target, paving the way for precision medicine in ALD, though further experimental validation is needed to establish their functional relevance.
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