ArticleMolecular biology reports2012
High levels of glucose induce "metabolic memory" in cardiomyocyte via epigenetic histone H3 lysine 9 methylation.
Article in Molecular biology reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 64 citations in OpenAlex.
- Engineering and Integrating Blood Vessel Organoids: a Comprehensive Blueprint for Physiological and Disease Modeling.Stem cell reviews and reports · 2026Review
- Nuclear N-glycosylation maintains H3K9me3 heterochromatin and genomic stability.Nature cell biology · 2026Article
- snRNA-seq identifies Fmo2npj metabolic health and disease · 2026Article
- Chronic hyperglycemia and cardiovascular dysfunction: an in-depth exploration of metabolic and cellular pathways in type 2 diabetes mellitus.Cardiovascular diabetology. Endocrinology reports · 2025Review
- Established and Emerging Roles of Epigenetic Regulation in Diabetic Cardiomyopathy.Diabetes/metabolism research and reviews · 2025Review
- Targeting Cellular Senescence: Pathophysiology in Multisystem Age-Related Diseases.Biomedicines · 2025Review
- Metabolic and Mitochondrial Dysregulations in Diabetic Cardiac Complications.International journal of molecular sciences · 2025Review
- Unveiling impaired vascular function and cellular heterogeneity in diabetic donor-derived vascular organoids.Stem cells (Dayton, Ohio) · 2024Article
- An update on chronic complications of diabetes mellitus: from molecular mechanisms to therapeutic strategies with a focus on metabolic memory.Molecular medicine (Cambridge, Mass.) · 2024Review
- Post-translational modifications in diabetic cardiomyopathy.Journal of cellular and molecular medicine · 2024Review
- Vascular organoids: unveiling advantages, applications, challenges, and disease modelling strategies.Stem cell research & therapy · 2023Review
- Epigenetics of methylation modifications in diabetic cardiomyopathy.Frontiers in endocrinology · 2023Review
- Targeting Epigenetic Regulation of Cardiomyocytes through Development for Therapeutic Cardiac Regeneration after Heart Failure.International journal of molecular sciences · 2022Review
- Epigenetic modifications in metabolic memory: What are the memories, and can we erase them?American journal of physiology. Cell physiology · 2022Review
- Integrative epigenomic and transcriptomic analyses reveal metabolic switching by intermittent fasting in brain.GeroScience · 2022Article
- Hyperglycemic memory in diabetic cardiomyopathy.Frontiers of medicine · 2022Review
- Review
- Inflamed adipose tissue: A culprit underlying obesity and heart failure with preserved ejection fraction.Frontiers in immunology · 2022Review
- Histone Methylation and Oxidative Stress in Cardiovascular Diseases.Oxidative medicine and cellular longevity · 2022Review
- The impact of reactive oxygen species in the development of cardiometabolic disorders: a review.Lipids in health and disease · 2021Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic patients continue to develop inflammation and cardiovascular complication even after achieving glycemic control, suggesting a "metabolic memory". Metabolic memory is a major challenge in the treatment of diabetic complication, and the mechanisms underlying metabolic memory are not clear. Recent studies suggest a link between chromatin histone methylation and metabolic memory. In this study, we tested whether histone 3 lysine-9 tri-methylation (H3K9me3), a key epigenetic chromatin marker, was involved in high glucose (HG)-induced inflammation and metabolic memory. Incubating cardiomyocyte cells in HG resulted in increased levels of inflammatory cytokine IL-6 mRNA when compared with myocytes incubated in normal culture media, whereas mannitol (osmotic control) has no effect. Chromatin immunoprecipitation (ChIP) assays showed that H3K9me3 levels were significantly decreased at the promoters of IL-6. Immunoblotting demonstrated that protein levels of the H3K9me3 methyltransferase, Suv39h1, were also reduced after HG treatment. HG-induced apoptosis, mitochondrial dysfunction and cytochrome-c release were reversible. However, the effects of HG on the expression of IL-6 and the levels of H3K9me3 were irreversible after the removal of HG from the culture. These results suggest that HG-induced sustained inflammatory phenotype and epigenetic histone modification, rather than HG-induced mitochondrial dysfunction and apoptosis, are main mechanisms responsible for metabolic memory. In conclusion, our data demonstrate that HG increases expression of inflammatory cytokine and decreases the levels of histone-3 methylation at the cytokine promoter, and suggest that modulating histone 3 methylation and inflammatory cytokine expression may be a useful strategy to prevent metabolic memory and cardiomyopathy in diabetic patients.
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