ArticleHepatology (Baltimore, Md.)2025
LncRNA H19 promoted alcohol-associated liver disease through dysregulation of alternative splicing and methionine metabolism.
Article in Hepatology (Baltimore, Md.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- LncRNA TUG1 promotes hepatic lipid accumulation by targeting the miR-29a-3p/SREBP-2/HMGCR axis in MAFLD.Functional & integrative genomics · 2026Article
- Autophagy in the liver.Autophagy reports · 2026Review
- Physiological Mechanisms Vulnerable to Alcohol-Induced Alterations: Role in Chronic Comorbidities.Comprehensive Physiology · 2025Review
- Non-coding RNAs in alcohol-associated liver disease.Liver research (Beijing, China) · 2025Review
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Authors and funding
11 authors.
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Abstract
BACKGROUND AND
aimsLong noncoding RNAs constitute a significant portion of the human genome. Among these, lncRNA H19, initially identified for its high expression during fetal development followed by a decline in the liver postnatally, re-emerges in various liver diseases. However, its specific role in alcohol-associated liver disease (ALD) remains unclear. APPROACH AND
resultsElevated H19 levels were detected in peripheral blood and livers of patients with alcohol-associated cirrhosis and hepatitis, as well as in livers of ethanol-fed mice. Hepatic overexpression of H19 exacerbated ethanol-induced liver steatosis and injury. Metabolomics analysis revealed decreased methionine levels in H19-overexpressed mouse livers, attributable to H19-mediated inhibition of betaine homocysteine methyltransferase (BHMT), a crucial enzyme in methionine synthesis. H19 regulated BHMT alternative splicing through polypyrimidine tract-binding protein 1 (PTBP1), resulting in a reduced Bhmt protein-coding variant. The maternally specific knockout of H19 ( H19Mat+/- ) or liver-specific knockout of the H19 differentially methylated domain ( H19DMDHep-/- ) in ethanol-fed mice upregulated BHMT expression and ameliorated hepatic steatosis. Furthermore, BHMT restoration counteracted H19-induced ethanol-mediated hepatic steatosis.
conclusionsThis study identifies a novel mechanism whereby H19, via PTBP1-mediated BHMT regulation, influences methionine metabolism in ALD. Targeting the H19-PTBP1-BHMT pathway may offer new therapeutic avenues for ALD.
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