ArticleThe Journal of biological chemistry2016
O-GlcNAcylation of 8-Oxoguanine DNA Glycosylase (Ogg1) Impairs Oxidative Mitochondrial DNA Lesion Repair in Diabetic Hearts.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 67 citations in OpenAlex.
- Early Cardiomyopathy in Prediabetic NDPK-B-Deficient Mice Is Associated with Remodeling of the Mitochondrial O-GlcNAc Proteome.International journal of molecular sciences · 2026Article
- Maternal hyperglycemia-induced O-GlcNAcylation of CaMKIIδ promotes mtDNA release and cardiac remodeling in offspring.Nature communications · 2026Article
- Is Type 2 Diabetes a Modifiable Risk Factor for the Evolution and Progression of Heart Failure With a Preserved Ejection Fraction?Journal of the American College of Cardiology · 2025Review
- Mitochondrial DNA Dysfunction in Cardiovascular Diseases: A Novel Therapeutic Target.Antioxidants (Basel, Switzerland) · 2025Review
- Global research trends in the relationship between diabetic cardiomyopathy and mitochondria: a bibliometric analysis.Hereditas · 2025Article
- Protein glycosylation in cardiovascular health and disease.Nature reviews. Cardiology · 2024Review
- Molecular Basis of Cardiomyopathies in Type 2 Diabetes.International journal of molecular sciences · 2024Review
- Semaglutide ameliorates cardiac remodeling in male mice by optimizing energy substrate utilization through the Creb5/NR4a1 axis.Nature communications · 2024Article
- IL-37 ameliorates myocardial fibrosis by regulating mtDNA-enriched vesicle release in diabetic cardiomyopathy mice.Journal of translational medicine · 2024Article
- Roles of O-GlcNAcylation in Mitochondrial Homeostasis and Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2024Review
- Post-translational modifications in diabetic cardiomyopathy.Journal of cellular and molecular medicine · 2024Review
- OGT and OGA: Sweet guardians of the genome.The Journal of biological chemistry · 2024Review
- O-GlcNAcylation: a pro-survival response to acute stress in the cardiovascular and central nervous systems.European journal of medical research · 2024Review
- Catalytic activity of OGG1 is impaired by Zinc deficiency.DNA repair · 2024Article
- Single-molecule analysis of purified proteins and nuclear extracts: Insights from 8-oxoguanine glycosylase 1.DNA repair · 2024Article
- ErZhiTianGui Decoction alleviates age-related ovarian aging by regulating mitochondrial homeostasis and inhibiting ferroptosis.Journal of ovarian research · 2024Article
- Review
- Novel insights into the role of mitochondria in diabetic cardiomyopathy: molecular mechanisms and potential treatments.Cell stress & chaperones · 2023Review
- The Extracellular Matrix Vitalizer RAAntioxidants (Basel, Switzerland) · 2023Article
- Potential clinical biomarkers and perspectives in diabetic cardiomyopathy.Diabetology & metabolic syndrome · 2023Review
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
mtDNA damage in cardiac myocytes resulting from increased oxidative stress is emerging as an important factor in the pathogenesis of diabetic cardiomyopathy. A prevalent lesion that occurs in mtDNA damage is the formation of 8-hydroxy-2'-deoxyguanosine (8-OHdG), which can cause mutations when not repaired properly by 8-oxoguanine DNA glycosylase (Ogg1). Although the mtDNA repair machinery has been described in cardiac myocytes, the regulation of this repair has been incompletely investigated. Here we report that the hearts of type 1 diabetic mice, despite having increased Ogg1 protein levels, had significantly lower Ogg1 activity than the hearts of control, non-type 1 diabetic mice. In diabetic hearts, we further observed increased levels of 8-OHdG and an increased amount of mtDNA damage. Interestingly, Ogg1 was found to be highly O-GlcNAcylated in diabetic mice compared with controls. In vitro experiments demonstrated that O-GlcNAcylation inhibits Ogg1 activity, which could explain the mtDNA lesion accumulation observed in vivo Reducing Ogg1 O-GlcNAcylation in vivo by introducing a dominant negative O-GlcNAc transferase mutant (F460A) restored Ogg1 enzymatic activity and, consequently, reduced 8-OHdG and mtDNA damage despite the adverse hyperglycemic milieu. Taken together, our results implicate hyperglycemia-induced O-GlcNAcylation of Ogg1 in increased mtDNA damage and, therefore, provide a new plausible biochemical mechanism for diabetic cardiomyopathy.
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