ArticleOxidative medicine and cellular longevity2022
Selenium Supplementation Improved Cardiac Functions by Suppressing DNMT2-Mediated
Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 31 citations in OpenAlex.
- Mechanistic Study of m5C Modification in Stem Cell Differentiation and Disease Regulation.Stem cell reviews and reports · 2026Review
- Apigenin, Selenium, and Combinations Are Effective in Preventing 5-Fluorouracil Induced Cardiovascular Damage.Journal of biochemical and molecular toxicology · 2026Article
- Review
- Effects of Diet Strategy and Nutrients on the Progression and Prevention of Diabetic Cardiomyopathy: A Narrative Review.Food science & nutrition · 2026Review
- A New Complexity Layer: DNA Methylation and the Predictive Impact of Epigenetic Tests.International journal of molecular sciences · 2026Review
- Cardiomyocyte programmed cell death in dilated cardiomyopathy: molecular crosstalk and therapeutic implications.Frontiers in cell and developmental biology · 2026Review
- Role and relevance of exosome-mediated epigenetic regulation in the pathogenesis, diagnosis and treatment of cardiovascular diseases (Review).Molecular medicine reports · 2026Review
- Integration of Multi-Omics Data Identifies the Role of the Selenium-Related Gene PNPO and Pre-exhausted CD127Cancer informatics · 2026Article
- Diabetic Atrial Cardiomyopathy: Pathogenesis, Diagnosis, Management, AI-Driven Diagnosis, and Risk Prediction.Journal of diabetes research · 2026Review
- Epigenetic Mechanisms in Heart Diseases.Reviews in cardiovascular medicine · 2025Review
- Review
- Genomic medicine and personalized treatment: a narrative review.Annals of medicine and surgery (2012) · 2025Review
- Melatonin alleviates aging-related heart failure through melatonin receptor 1A/B knockout in mice.Heliyon · 2024Article
- Evaluating the link between DIO3-FA27 promoter methylation, biochemical indices, and heart failure progression.Clinical epigenetics · 2024Article
- Epigenetics in diabetic cardiomyopathy.Clinical epigenetics · 2024Review
- Diabetic Retinopathy and Regulation of Mitochondrial Glutathione-Glutathione Peroxidase Axis in Hyperhomocysteinemia.Antioxidants (Basel, Switzerland) · 2024Article
- Inflammation in Heart Failure-Future Perspectives.Journal of clinical medicine · 2023Review
- Article
- Review
- Selenium deficiency causes hypertension by increasing renal ATFree radical biology & medicine · 2023Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Advanced glycation end products (AGEs) are featured metabolites associated with diabetic cardiomyopathy which is characterized by heart failure caused by myocyte apoptosis. Selenium was proved cardioprotective. This study was aimed at investigating the therapeutic effects and underlying mechanisms of selenium supplementation on AGE-induced heart failure. Methods: Rats and primary myocytes were exposed to AGEs. Selenium supplementation was administrated. Cardiac functions and myocyte apoptosis were evaluated. Oxidative stress was assessed by total antioxidant capacity (TAC), reactive oxygen species (ROS) generation, and GPX activity. Expression levels of DNA methyltransferases (DNMTs) and glutathione peroxidase 1 (GPX1) were evaluated. DNA methylation of the GPX1 promoter was analyzed. Results: AGE exposure elevated intracellular ROS generation, induced myocyte apoptosis, and impaired cardiac functions. AGE exposure increased DNMT1 and DNMT2 expression, leading to the reduction of GPX1 expression and activity in the heart. Selenium supplementation decreased DNMT2 expression, recovered GPX1 expression and activity, and alleviated intracellular ROS generation and myocyte apoptosis, resulting in cardiac function recovery. DNA methylation analysis in primary myocytes indicated that selenium supplementation or DNMT inhibitor AZA treatment reduced DNA methylation of the GPX1 gene promoter. Selenium supplementation and AZA administration showed synergic inhibitory effect on GPX1 gene promoter methylation. Conclusions: Selenium supplementation showed cardioprotective effects on AGE-induced heart failure by suppressing ROS-mediated myocyte apoptosis. Selenium supplementation suppressed ROS generation by increasing GPX1 expression via inhibiting DNMT2-induced GPX1 gene promoter DNA methylation in myocytes exposed to AGEs.
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