ArticleToxicological sciences : an official journal of the Society of Toxicology2018
Modulation of O-GlcNAc Levels in the Liver Impacts Acetaminophen-Induced Liver Injury by Affecting Protein Adduct Formation and Glutathione Synthesis.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- FBXO31-mediated ubiquitination of OGT maintains O-GlcNAcylation homeostasis to restrain endometrial malignancy.Nature communications · 2025Article
- An Efficient and Accessible Hectogram-Scale Synthesis for the Selective O-GlcNAcase Inhibitor Thiamet-G.ACS omega · 2024Article
- Protein posttranslational modifications in metabolic diseases: basic concepts and targeted therapies.MedComm · 2024Review
- Review
- Aberrant mitochondrial aggregation of TDP-43 activated mitochondrial unfolded protein response and contributed to recovery of acetaminophen induced acute liver injury.Toxicology research · 2024Article
- Emerging Role of Protein O-GlcNAcylation in Liver Metabolism: Implications for Diabetes and NAFLD.International journal of molecular sciences · 2023Review
- O-GlcNAc regulates the mitochondrial integrated stress response by regulating ATF4.Frontiers in aging neuroscience · 2023Article
- O-GlycNacylation Remission Retards the Progression of Non-Alcoholic Fatty Liver Disease.Cells · 2022Review
- Regulation of Liver Regeneration by Hepatocyte O-GlcNAcylation in Mice.Cellular and molecular gastroenterology and hepatology · 2022Article
- Hepatocyte-Specific Deletion of Yes-Associated Protein Improves Recovery From Acetaminophen-Induced Acute Liver Injury.Toxicological sciences : an official journal of the Society of Toxicology · 2021Article
- Role ofPhysiological reviews · 2021Review
- Acetaminophen Test Battery (ATB): A Comprehensive Method to Study Acetaminophen-Induced Acute Liver Injury.Gene expression · 2020Review
- OGA Inhibition Alters Energetics and Nutrient Sensing in Alzheimer's Disease Cytoplasmic Hybrids.Journal of Alzheimer's disease : JAD · 2020Article
- GLT25D2 Is Critical for Inflammatory Immune Response to Promote Acetaminophen-Induced Hepatotoxicity by Autophagy Pathway.Frontiers in pharmacology · 2020Article
- O-GlcNAc transferase suppresses necroptosis and liver fibrosis.JCI insight · 2019Article
- Disruption of O-GlcNAc homeostasis during mammalian oocyte meiotic maturation impacts fertilization.Molecular reproduction and development · 2019Article
- Liver Regeneration after Acetaminophen Hepatotoxicity: Mechanisms and Therapeutic Opportunities.The American journal of pathology · 2019Review
- A Novel Mechanism of Starvation-Stimulated Hepatic Autophagy: Calcium-Induced O-GlcNAc-Dependent Signaling.Hepatology (Baltimore, Md.) · 2019Article
- Hepatoprotective Effect of Baicalein Against Acetaminophen-Induced Acute Liver Injury in Mice.Molecules (Basel, Switzerland) · 2018Article
- Critical observations that shaped our understanding of the function(s) of intracellular glycosylation (O-GlcNAc).FEBS letters · 2018Review
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
Overdose of acetaminophen (APAP) results in acute liver failure. We have investigated the role of a posttranslational modification of proteins called O-GlcNAcylation, where the O-GlcNAc transferase (OGT) adds and O-GlcNAcase (OGA) removes a single β-D-N-acetylglucosamine (O-GlcNAc) moiety, in the pathogenesis of APAP-induced liver injury. Hepatocyte-specific OGT knockout mice (OGT KO), which have reduced O-GlcNAcylation, and wild-type (WT) controls were treated with 300 mg/kg APAP and the development of injury was studied over a time course from 0 to 24 h. OGT KO mice developed significantly lower liver injury as compared with WT mice. Hepatic CYP2E1 activity and glutathione (GSH) depletion following APAP treatment were not different between WT and OGT KO mice. However, replenishment of GSH and induction of GSH biosynthesis genes were significantly faster in the OGT KO mice. Next, male C57BL/6 J mice were treated Thiamet-G (TMG), a specific inhibitor of OGA to induce O-GlcNAcylation, 1.5 h after APAP administration and the development of liver injury was studied over a time course of 0-24 h. TMG-treated mice exhibited significantly higher APAP-induced liver injury. Treatment with TMG did not affect hepatic CYP2E1 levels, GSH depletion, APAP-protein adducts, and APAP-induced mitochondrial damage. However, GSH replenishment and GSH biosynthesis genes were lower in TMG-treated mice after APAP overdose. Taken together, these data indicate that induction in cellular O-GlcNAcylation exacerbates APAP-induced liver injury via dysregulation of hepatic GSH replenishment response.
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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.