ArticleScientific reports2025
METTL3 promotes the progression of non-alcoholic fatty liver disease by mediating m6A methylation of FAS.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Zfp217 Regulates Hepatic de Novo Lipogenesis via METTL3-Mediated N6-Methyladenosine Modification of SREBF1.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- The METTL3/TRIM37 axis contributes to the progression of non-alcoholic fatty liver disease by promoting CAV1 degradation.Molecular and cellular biochemistry · 2026Article
- Oroxylin A ameliorates hepatic steatosis and non-alcoholic fatty liver disease through the regulation of CPT1A mBiochemistry and biophysics reports · 2026Article
- Pre-clinical anti-tumor activity and preliminary safety of METTL3 inhibitors STM2457 and UZH1a in neuroblastoma.Translational cancer research · 2026Article
- Epitranscriptomic modifications in programmed cell death: mechanistic insights and implications for liver diseases.Cellular & molecular biology letters · 2025Review
- N6-Methyladenosine Modification in the Metabolic Dysfunction-Associated Steatotic Liver Disease.Nutrients · 2025Review
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N6-methyladenosine (m6A) is involved in the development of non-alcoholic fatty liver disease (NAFLD). Here, we aimed to investigate the effect of m6A methyltransferase METTL3 on liver damage in high-fat diet (HFD)-induced mouse model and hepatocyte damage treated with free fatty acid (FFA). Plasma lipid, lipogenesis, viability, and apoptosis were measured to assess injury. m6A methylation was evaluated using m6A dot blot, methylated RNA immunoprecipitation, dual-luciferase reporter assay, and RNA decay assay. The results indicated that METTL3 was highly expressed in the liver of HFD mice, which knockdown improved plasma lipid and reduced liver lipids. Additionally, silencing of METTL3 promoted cell viability, inhibited apoptosis, reduced lipid concentrations, and downregulated lipogenesis-related marker levels. Moreover, METTL3 promoted the m6A methylation of FAS and enhanced its stability. In conclusion, silencing of METTL3 attenuates the progression of NAFLD by FAS m6A methylation, suggesting that METTL3 may be a promising target for treating NAFLD.
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