{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Hong SH"],"funding":["Department of Environmental Sciences","NIAAA NIH HHS","Yale School of Public Health, Yale University","National Institutes of Health"],"pagination":["111093"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11223951"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["398"],"pubmed_abstract":["Oxidative stress is intimately involved in the pathogenesis of fatty liver disease (FLD). A major factor contributing to oxidative stress is the depletion of the ubiquitous antioxidant glutathione (GSH). Unexpectedly, chronic GSH deficiency renders glutamate-cysteine ligase modifier subunit (Gclm)-null mice protected from fatty liver injuries. Epigenetic regulation serves as an important cellular mechanism in modulating gene expression and disease outcome in FLD, although it is not well understood how systemic redox imbalance modifies the liver epigenome. In the current study, utilizing the Gclm-null mouse model, we aimed to elucidate redox-associated epigenomic changes and their implications in liver stress response. We performed high-throughput array-based DNA methylation profiling (MeDI"],"journal":["Chemico-biological interactions"],"pubmed_title":["Liver epigenomic signature associated with chronic oxidative stress in a mouse model of glutathione deficiency."],"pmcid":["PMC11223951"],"funding_grant_id":["K01AA025093","K01 AA025093","R01 AA028859","R01AA028859"],"pubmed_authors":["Zhu Y","Chen Y","Hong SH","Yu X"],"additional_accession":[]},"is_claimable":false,"name":"Liver epigenomic signature associated with chronic oxidative stress in a mouse model of glutathione deficiency.","description":"Oxidative stress is intimately involved in the pathogenesis of fatty liver disease (FLD). A major factor contributing to oxidative stress is the depletion of the ubiquitous antioxidant glutathione (GSH). Unexpectedly, chronic GSH deficiency renders glutamate-cysteine ligase modifier subunit (Gclm)-null mice protected from fatty liver injuries. Epigenetic regulation serves as an important cellular mechanism in modulating gene expression and disease outcome in FLD, although it is not well understood how systemic redox imbalance modifies the liver epigenome. In the current study, utilizing the Gclm-null mouse model, we aimed to elucidate redox-associated epigenomic changes and their implications in liver stress response. We performed high-throughput array-based DNA methylation profiling (MeDI","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Aug","modification":"2026-03-18T13:34:50.198Z","creation":"2025-08-18T09:54:17.309Z"},"accession":"S-EPMC11223951","cross_references":{"pubmed":["38830566"],"doi":["10.1016/j.cbi.2024.111093"]}}