ArticleExperimental and molecular pathology2014
Mallory-Denk Body (MDB) formation modulates Ufmylation expression epigenetically in alcoholic hepatitis (AH) and non-alcoholic steatohepatitis (NASH).
Article in Experimental and molecular pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Pooled it
- UFMylation in lipid metabolism disorders-associated diseases.Molecular biology reports · 2026Review
- Ubiquitination and ubiquitin-like modifications in metabolic dysfunction-associated steatotic liver disease: mechanisms and implications.BMB reports · 2025Review
- Studies on the functional role of UFMylation in cells (Review).Molecular medicine reports · 2025Review
- Article
- Review
- Post-translational modifications of histone and non-histone proteins in epigenetic regulation and translational applications in alcohol-associated liver disease: Challenges and research opportunities.Pharmacology & therapeutics · 2023Review
- Non-Classical HLA Class 1b and Hepatocellular Carcinoma.Biomedicines · 2023Review
- Dysregulation of PD-L1 by UFMylation imparts tumor immune evasion and identified as a potential therapeutic target.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Epigenetics of alcohol-related liver diseases.JHEP reports : innovation in hepatology · 2022Review
- The case for FAT10 as a novel target in fatty liver diseases.Frontiers in pharmacology · 2022Review
- Highly Specialized Ubiquitin-Like Modifications: Shedding Light into the UFM1 Enigma.Biomolecules · 2021Review
- The Role of Epigenetic Changes in the Progression of Alcoholic Steatohepatitis.Frontiers in physiology · 2021Review
- The Role of FAT10 in Alcoholic Hepatitis Pathogenesis.Biomedicines · 2020Review
- Alcoholic-Hepatitis, Links to Brain and Microbiome: Mechanisms, Clinical and Experimental Research.Biomedicines · 2020Review
- The UFMylation System in Proteostasis and Beyond.Trends in cell biology · 2019Review
- Silybin Alleviates Hepatic Steatosis and Fibrosis in NASH Mice by Inhibiting Oxidative Stress and Involvement with the Nf-κB Pathway.Digestive diseases and sciences · 2018Article
- LncRNA-SVUGP2 suppresses progression of hepatocellular carcinoma.Oncotarget · 2017Article
- The role of Tec kinase signaling pathways in the development of Mallory Denk Bodies in balloon cells in alcoholic hepatitis.Experimental and molecular pathology · 2017Article
- Role of Protein Quality Control Failure in Alcoholic Hepatitis Pathogenesis.Biomolecules · 2017Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Promoter CpG island hypermethylation is an important mechanism for inactivating key cellular enzymes that mediate epigenetic processes in hepatitis-related hepatocellular carcinoma (HCC). The ubiquitin-fold modifier 1 (Ufm1) conjugation pathway (Ufmylation) plays an essential role in protein degradation, protein quality control and signal transduction. Previous studies showed that the Ufmylation pathway was downregulated in alcoholic hepatitis (AH), non-alcoholic steatohepatitis (NASH) and in mice fed DDC, resulting in the formation of Mallory-Denk Bodies (MDBs). In this study, we further discovered that betaine, a methyl donor, fed together with DDC significantly prevents the increased expression of Ufmylation in drug-primed mice fed DDC. Betaine significantly prevented transcript silencing of Ufm1, Uba5 and UfSP1 where MDBs developed and also prevented the increased expression of FAT10 and LMP7 caused by DDC re-fed mice. Similar downregulation of Ufmylation was observed in multiple AH and NASH biopsies which had formed MDBs. The DNA methylation levels of Ufm1, Ufc1 and UfSP1 in the promoter CpG region were significantly increased both in AH and NASH patients compared to normal subjects. DNA (cytosine-5-)-methyltransferase 1 (DNMT1) and DNA (cytosine-5-)-methyltransferase 3 beta (DNMT3B) mRNA levels were markedly upregulated in AH and NASH patients, implying that the maintenance of Ufmylation methylation might be mediated by DNMT1 and DNMT3B together. These data show that MDB formation results from Ufmylation expression epigenetically in AH and NASH patients. Promoter CpG methylation may be a major mechanism silencing Ufmylation expression.
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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.