ArticleBMC biology2025
O-GlcNAcylation attenuates ischemia-reperfusion-induced pulmonary epithelial cell ferroptosis via the Nrf2/G6PDH pathway.
Article in BMC biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- The landscape of protein post-translational modifications in the pathogenesis of acute respiratory distress syndrome.Journal of thoracic disease · 2026Review
- Magnetic Fields in Cancer Therapy: Mechanistic Insights, Signaling Pathways, and Evidence from Clinical and In Vitro Studies.Pharmaceutics · 2026Review
- OGT-mediated O-GlcNAcylation Protects Against Myocardial Ischemia-Reperfusion Injury via Targeting MG53.Applied biochemistry and biotechnology · 2026Article
- Ferroptosis-driven metabolic reprogramming in macrophages: Reshaping glucose utilization landscapes.Chinese medical journal · 2026Review
- Lactylation-driven PDLIM1/PDAP1 axis remodels the inflammatory landscape of acute lung injury: mechanistic insights and precision intervention.Frontiers in immunology · 2026Article
- O-GlcNAcylation in novel regulated cell death: ferroptosis, pyroptosis, and necroptosis.Cell death discovery · 2025Review
- Article
- Multi-omics integration reveals YWHAE as a key mediator of ferroptosis in ARDS.Functional & integrative genomics · 2025Article
- Combinational Analysis of Metabolomic and O-GlcNAcylation Omics Reveals the HBP Metabolic Regulation of Chemoresistance via GFPT1/NR3C1 O-GlcNAcylation/GPX4 Axis.Research (Washington, D.C.) · 2025Article
- Astragalus Polysaccharide Suppresses Inflammation and Promotes Apoptosis in Hypertrophic Scars by Suppressing OGT-Mediated Nrf2 O-GlcNAcylation.Iranian journal of pharmaceutical research : IJPRArticle
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8 authors.
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Abstract
backgroundLung ischemia-reperfusion (I/R) injury is a common clinical pathology associated with high mortality. The pathophysiology of lung I/R injury involves ferroptosis and elevated protein O-GlcNAcylation levels, while the effect of O-GlcNAcylation on lung I/R injury remains unclear. This research aimed to explore the effect of O-GlcNAcylation on reducing ferroptosis in pulmonary epithelial cells caused by I/R.
resultsFirst, we identified O-GlcNAc transferase 1 (Ogt1) as a differentially expressed gene in lung epithelial cells of acute lung injury/acute respiratory distress syndrome (ALI/ARDS) patients, using single-cell sequencing, and Gene Ontology analysis (GO analysis) revealed the enrichment of the ferroptosis process. We found a time-dependent dynamic alteration in lung O-GlcNAcylation during I/R injury. Proteomics analysis identified the differentially expressed proteins enriched in ferroptosis and multiple redox-related pathways based on KEGG annotation. Thus, we generated Ogt1-conditional knockout mice and found that Ogt1 deficiency aggravated ferroptosis, as evidenced by lipid reactive oxygen species (lipid ROS), malondialdehyde (MDA), Fe
conclusionsIn summary, we revealed that O-GlcNAcylation could protect against I/R lung injury by reducing ferroptosis sensitivity via the Nrf2/G6PDH pathway. Our work will provide a new basis for clinical therapeutic strategies for pulmonary ischemia-reperfusion-induced acute lung injury.
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