ArticleCardiovascular toxicology2023
Liraglutide Attenuates Myocardial Ischemia/Reperfusion Injury Through the Inhibition of Necroptosis by Activating GLP-1R/PI3K/Akt Pathway.
Article in Cardiovascular toxicology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 23 citations in OpenAlex.
- A systematic review and meta-analyses of glucagon-like peptide-1 receptor agonists in acute myocardial infarction.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2026Review
- GLP-1 Receptor Agonists in the Rehabilitation of Patients with Heart Failure: Mechanisms, Clinical Evidence, and Future Perspectives.Nutrients · 2026Review
- GLP-1 Receptor Agonists in Chronic Inflammatory Skin Diseases: Immunometabolic Mechanisms and Translational Perspectives.Pharmaceutics · 2026Review
- Semaglutide ameliorates coronary microembolization-induced injury by suppressing apoptosis and inflammation via the HMGB1/RAGE/NF-κB p65 pathway.Journal of geriatric cardiology : JGC · 2026Article
- GLP-1 and the cardiovascular system.The Journal of clinical investigation · 2026Review
- Molecular and Cellular Mechanisms of Myocardial Ischemia and Reperfusion Injury: A Narrative Review.Cells · 2026Review
- Traditional Chinese Medicine Treatment for Coronary Heart Disease: Pathological Mechanisms of Modulating Cell Death Pathways.Journal of inflammation research · 2026Review
- Evaluating Semaglutide's Protection in H/R - Injured AC16 Cardiomyocytes: Oxidative Stress, Inflammation, Apoptosis, and Autophagy Insights.International journal of general medicine · 2026Article
- Potential Antiarrhythmic Mechanisms of Glucagon-Like Peptide-1 Receptor Agonists (GLP-1RAs).Drug design, development and therapy · 2026Review
- Ginkgolide C Improves Cardiac Function and Ameliorates Myocardial Ischemia/Reperfusion Injury by Regulating PI3K/Akt Pathway.Physiological research · 2025Article
- Emerging therapy strategies for energy metabolism in acute myocardial infarction.Journal of translational medicine · 2025Review
- Research Progress on the Association Between GLP-1 Receptor Agonists and Cardiomyopathy.Reviews in cardiovascular medicine · 2025Review
- Programmed Cell Death in Heart Failure: Mechanisms, Impacts, and Therapeutic Prospects.Reviews in cardiovascular medicine · 2025Review
- Mitochondrial Ferritin Overexpression Attenuates Ferroptosis and Mitochondrial Dysfunction by Reducing VDAC1 to Relieve MI/RI-Induced Damage.Journal of cellular and molecular medicine · 2025Article
- The GLP-1 receptor agonist liraglutide inhibits necroptosis and neuroinflammation in a mouse model of Parkinson's disease with diabetes co-morbidity.Frontiers in neuroscience · 2025Article
- Sevoflurane Alleviates Cardiomyocyte Ferroptosis via Ubiquitin-Specific Protease 7/Phosphatase and Tensin Homolog Modulation.Drug design, development and therapy · 2025Article
- Mechanisms and Therapeutic Potential of Multiple Forms of Cell Death in Myocardial Ischemia-Reperfusion Injury.International journal of molecular sciences · 2024Review
- [MiR-224-5p overexpression inhibits oxidative stress by regulating the PI3K/Akt/FoxO1 axis to attenuate hypoxia/reoxygenation-induced cardiomyocyte injury].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Peptides Are Cardioprotective Drugs of the Future: The Receptor and Signaling Mechanisms of the Cardioprotective Effect of Glucagon-like Peptide-1 Receptor Agonists.International journal of molecular sciences · 2024Review
- Glucagon-like peptide-1 receptor agonists: new strategies and therapeutic targets to treat atherosclerotic cardiovascular disease.Frontiers in pharmacology · 2024Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Necroptosis is a crucial programmed cell death that is tightly associated with myocardial ischemia/reperfusion injury (MI/RI). Liraglutide is an effective option for the treatment of type 2 diabetes and has recently been reported to exert cardioprotective effects on MI/RI. Researchers do not know whether the cardioprotective effect of liraglutide is involved in regulating necroptosis. This study aimed to explore the effect of liraglutide on MI/RI-induced necroptosis and its potential mechanisms. Hypoxia/reoxygenation (H/R) was performed on H9c2 cells in vitro to simulate ischemia/reperfusion (I/R) injury, and an MI/RI rat model was established in vivo by ligating the anterior descending branch of the left coronary artery. H/R or I/R damage was assessed by performing biochemical assay, Hoechst 33342/PI staining, H&E (hematoxylin and eosin) staining, and Annexin-V/PI staining. Our data revealed that liraglutide resulted in markedly increased cell viability and reduced cardiac enzyme release by protecting cardiomyocytes from a necrosis-like phenotype after H/R. The myocardial infarct size and cardiac enzyme release were reduced in the heart tissues from the liraglutide-treated group. The levels of necroptosis-associated proteins (receptor-interacting protein kinase 3 (RIPK3), p-RIPK3, and phosphorylated-mixed lineage kinase domain-like protein (p-MLKL)) were also reduced by the liraglutide treatment. Mechanistically, we revealed that liraglutide exerted cardioprotective effects through a glucagon-like peptide-1 receptor (GLP-1R) and phosphatidylinositol-3 kinase (PI3K)-dependent pathway. Both the GLP-1R inhibitor exendin (9-39) and the PI3K inhibitor LY294002 abrogated the protective effects of liraglutide in vitro. We found that liraglutide may attenuate MI/RI by inhibiting necroptosis, in part by enhancing the activity of the GLP-1R/PI3K/Akt pathway.
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