biostudies-literatureLi TDoctoral Fund of Jining No.1 People's HospitalProjects of medical and health technology development program in Shandong provinceNatural Science Research Project of Universities in Jiangsu ProvinceKey Research and Development Program of Jining Science and TechnologyGeneral Program of China Postdoctoral Science FoundationSuzhou Science and Technology CouncilNatural Science Foundation of Jiangsu Provincee2307648https://www.ebi.ac.uk/biostudies/studies/S-EPMC10870076biostudies-literatureUnknown11(7)T-2 toxin causes renal dysfunction with proteinuria and glomerular podocyte damage. This work explores the role of metabolic disorder/reprogramming-mediated epigenetic modification in the progression of T-2 toxin-stimulated podocyte injury. A metabolomics experiment is performed to assess metabolic responses to T-2 toxin infection in human podocytes. Roles of protein O-linked-N-acetylglucosaminylation (O-GlcNAcylation) in regulating T-2 toxin-stimulated podocyte injury in mouse and podocyte models are assessed. O-GlcNAc target proteins are recognized by mass spectrometry and co-immunoprecipitation experiments. Moreover, histone acetylation and autophagy levels are measured. T-2 toxin infection upregulates glucose transporter type 1 (GLUT1) expression and enhances hexosamine biosynthetic paAdvanced science (Weinheim, Baden-Wurttemberg, Germany)T-2 Toxin-Mediated β-Arrestin-1 O-GlcNAcylation Exacerbates Glomerular Podocyte Injury via Regulating Histone Acetylation.PMC108700762022M711369BK202210912022YXNS1182021-BS-008SNG20190720KJB330002202113050502He CLi TZhang JChang TChen YSun WZhu SfalseT-2 Toxin-Mediated β-Arrestin-1 O-GlcNAcylation Exacerbates Glomerular Podocyte Injury via Regulating Histone Acetylation.T-2 toxin causes renal dysfunction with proteinuria and glomerular podocyte damage. This work explores the role of metabolic disorder/reprogramming-mediated epigenetic modification in the progression of T-2 toxin-stimulated podocyte injury. A metabolomics experiment is performed to assess metabolic responses to T-2 toxin infection in human podocytes. Roles of protein O-linked-N-acetylglucosaminylation (O-GlcNAcylation) in regulating T-2 toxin-stimulated podocyte injury in mouse and podocyte models are assessed. O-GlcNAc target proteins are recognized by mass spectrometry and co-immunoprecipitation experiments. Moreover, histone acetylation and autophagy levels are measured. T-2 toxin infection upregulates glucose transporter type 1 (GLUT1) expression and enhances hexosamine biosynthetic pa2024-01-01T00:00:00Z2024 Feb2026-06-12T05:50:40.007Z2025-04-05T09:07:16.008ZS-EPMC108700763808397510.1002/advs.202307648