ArticleEndocrine2024
Semaglutide attenuates pathological electrophysiological remodeling in diabetic cardiomyopathy via restoring Cx43 expression.
Article in Endocrine, 2024. 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, 9 citations in OpenAlex.
- Melatonin Attenuates Glucolipotoxicity-Induced Cardiac Oxidative Stress, Inflammation, Pyroptosis, and Fibrotic Remodeling in STZ/HFD-Treated ApoEAntioxidants (Basel, Switzerland) · 2026Article
- Clinical Impact of Semaglutide Beyond Glycemic Control: A Critical Analysis of Oncogenic Potential and Mitigation of Cardiotoxicity.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Chronic quercetin supplementation modulates cardiac function and signaling pathways in aged male Wistar rat hearts subjected to ischemia-reperfusion.Frontiers in cardiovascular medicine · 2026Article
- Potential Antiarrhythmic Mechanisms of Glucagon-Like Peptide-1 Receptor Agonists (GLP-1RAs).Drug design, development and therapy · 2026Review
- Research Progress on the Association Between GLP-1 Receptor Agonists and Cardiomyopathy.Reviews in cardiovascular medicine · 2025Review
- The landscape of novel antidiabetic drugs in diabetic HFpEF: relevant mechanisms and clinical implications.Cardiovascular diabetology · 2025Review
- Unveiling the Therapeutic Potential of the Second-Generation Incretin Analogs Semaglutide and Tirzepatide in Type 1 Diabetes and Latent Autoimmune Diabetes in Adults.Journal of clinical medicine · 2025Review
- Efficacy of Semaglutide in Modulating Cardiac Remodeling in Mice: A Review of Mechanisms and Outcomes.Research in heart yield and translational medicine · 2025Review
- Spotlight on the Mechanism of Action of Semaglutide.Current issues in molecular biology · 2024Review
- Research Progress on Peptide Drugs for Type 2 Diabetes and the Possibility of Oral Administration.Pharmaceutics · 2024Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundSemaglutide is a relatively new anti-hyperglycemic agent that was shown to carry cardioprotective potentials. However, the exact effects of semaglutide on diabetic cardiomyopathy (DCM) and their underlining mechanism remain unclear. This study aimed to evaluate the effects of semaglutide on myocardium injury and cardiac function in DCM mice and its potential mechanisms, with emphasis on its effects on Cx43 and electrophysiological remodeling.
methodsC57BL/6 mice were randomly divided into four groups: control group, semaglutide group, diabetes group, and diabetes + semaglutide treatment group. Type 1 diabetes were induced by intraperitoneal injection of streptozotocin. Mice in the semaglutide intervention group were injected subcutaneously with semaglutide (0.15 mg/kg) every week for 8 weeks. The blood glucose, cardiac function, oxidative stress markers, apoptosis, expression of Sirt1, AMPK, Cx43, and electrocardiogram of mice in each group were evaluated.
resultsTreatment with semaglutide alleviated glucose metabolism disorders and improved cardiac dysfunction in diabetic mice. In addition, semaglutide ameliorated the increase in oxidative stress and apoptosis in diabetic heart. Sirt1/AMPK pathway was activated after semaglutide treatment. Furthermore, diabetic mice showed reduced expression of Cx43 in the myocardium, accompanied by changes in electrocardiogram, including significantly prolonged RR, QRS, QT and QTc interval. Semaglutide treatment restored Cx43 expression and reversed the above-mentioned ECG abnormalities.
conclusionsOur research results showed that semaglutide protected against oxidative stress and apoptosis in diabetic heart, thereby improving cardiac function and electrophysiological remodelling in DCM mice, which may attribute to activation of Sirt1/AMPK pathway and restore of Cx43 expression.
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