ArticleThe American journal of pathology2017
Regulation of Cellular Senescence by miR-34a in Alcoholic Liver Injury.
Article in The American journal of pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
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Who cites it
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.
- Non-coding RNAs participate in interactions between senescence and gastrointestinal cancers.Frontiers in genetics · 2024Pooled it
- MicroRNA Dysregulation and Hepatic Involvement in Alcohol-Related Macrocytic Anaemia: Links to Severity Without Predictive Value for Treatment Response.Life (Basel, Switzerland) · 2026Article
- Cellular senescence in liver diseases: From molecular drivers to therapeutic targeting.Journal of hepatology · 2026Review
- Role of cellular senescence in hepatic diseases (Review).International journal of molecular medicine · 2025Review
- Hepatocyte delivery of miR-34b/c reduces hepatic stellate cell activation and improves liver fibrosis.Molecular therapy. Nucleic acids · 2025Article
- Non-coding RNAs in alcohol-associated liver disease.Liver research (Beijing, China) · 2025Review
- Portal Fibrosis and the Ductular Reaction: Pathophysiological Role in the Progression of Liver Disease and Translational Opportunities.Gastroenterology · 2025Review
- MASH as an emerging cause of hepatocellular carcinoma: current knowledge and future perspectives.Molecular oncology · 2025Review
- Molecular regulators of alcoholic liver disease: a comprehensive analysis of microRNAs and long non-coding RNAs.Frontiers in medicine · 2025Review
- Noncoding RNA and Alcohol Use Disorder: A Scoping Review of Current Research and Knowledge Gaps.Alcohol research : current reviews · 2025Article
- Binge ethanol exposure in advanced age elevates neuroinflammation and early indicators of neurodegeneration and cognitive impairment in female mice.Brain, behavior, and immunity · 2024Article
- Prenatal cigarette smoke exposure sensitizes acetaminophen-induced liver injury by modulating miR-34a-5p in male offspring mice.Frontiers in cell and developmental biology · 2024Article
- Alcohol-related liver disease (ALD): current perspectives on pathogenesis, therapeutic strategies, and animal models.Frontiers in pharmacology · 2024Review
- MiRNAs in Alcohol-Related Liver Diseases and Hepatocellular Carcinoma: A Step toward New Therapeutic Approaches?Cancers · 2023Review
- The senescent secretome drives PLVAP expression in cultured human hepatic endothelial cells to promote monocyte transmigration.iScience · 2023Article
- Enhanced CaNature communications · 2023Article
- Cholangiokines: undervalued modulators in the hepatic microenvironment.Frontiers in immunology · 2023Review
- The Male-Biased Expression of miR-2954 Is Involved in the Male Pathway of Chicken Sex Differentiation.Cells · 2022Article
- Tackling cellular senescence by targeting miRNAs.Biogerontology · 2022Review
- Epigenetics of alcohol-related liver diseases.JHEP reports : innovation in hepatology · 2022Review
Corrections and comments
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Authors and funding
17 authors at 7 institutions in 2 countries.
Funding
Abstract
Alcoholic liver disease remains a major cause of liver-related morbidity and mortality, which ranges from alcoholic steatohepatitis to fibrosis/cirrhosis and hepatocellular carcinoma, and the related mechanisms are understood poorly. In this study, we aimed to investigate the role of miR-34a in alcohol-induced cellular senescence and liver fibrosis. We found that hepatic miR-34a expression was upregulated in ethanol-fed mice and heavy drinkers with steatohepatitis compared with respective controls. Mice treated with miR-34a Vivo-Morpholino developed less severe liver fibrosis than wild-type mice after 5 weeks of ethanol feeding. Further mechanism exploration showed that inhibition of miR-34a increased cellular senescence of hepatic stellate cells (HSCs) in ethanol-fed mice, although it decreased senescence in total liver and hepatocytes, which was verified by the changes of senescence-associated β-galactosidase and gene expression. Furthermore, enhanced cellular senescence was observed in liver tissues from steatohepatitis patients compared with healthy controls. In addition, the expression of transforming growth factor-β1, drosophila mothers against decapentaplegic protein 2 (Smad2), and Smad3 was decreased after inhibition of miR-34a in ethanol-fed mice. Our in vitro experiments showed that silencing of miR-34a partially blocked activation of HSCs by lipopolysaccharide and enhanced senescence of HSCs. Furthermore, inhibition of miR-34a decreased lipopolysaccharide-induced fibrotic gene expression in cultured hepatocytes. In conclusion, our data suggest that miR-34a functions as a profibrotic factor that promotes alcohol-induced liver fibrosis by reducing HSC senescence and increasing the senescence of hepatocytes.
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Registered trials
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