ArticleFrontiers in pharmacology2025
Semaglutide attenuates myocardial ischemia-reperfusion injury by inhibiting ferroptosis of cardiomyocytes via activation of PKC-S100A9 axis.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Semaglutide alleviates ovarian ferroptosis in polycystic ovary syndrome and is associated with reduced GPX4 promoter hypermethylation.Journal of molecular histology · 2026Article
- GLP-1 and the cardiovascular system.The Journal of clinical investigation · 2026Review
- BACH1-CHAC1-Glutathione Axis Aggravates Myocardial Ischemia-Reperfusion Injury by Enhancing Ferroptosis and Oxidative Stress.Antioxidants (Basel, Switzerland) · 2026Article
- Evaluating Semaglutide's Protection in H/R - Injured AC16 Cardiomyocytes: Oxidative Stress, Inflammation, Apoptosis, and Autophagy Insights.International journal of general medicine · 2026Article
- A Comprehensive Review on the Cardioprotective and Nephroprotective Effects of Semaglutide, and Its Therapeutic Efficacy and Mechanisms in Cardiorenal Syndrome.Drug design, development and therapy · 2026Review
- GLP-1 Receptor Agonists in Heart Failure.Biomolecules · 2025Review
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Authors and funding
8 authors.
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Abstract
Objective: The incidence of ischemic cardiomyopathy increases annually worldwide, and it is the leading cause of mortality in China. Although interventional diagnostic and therapeutic techniques can promptly open the culprit vessels, myocardial ischemia-reperfusion injury (MIRI), resulting from restored blood flow, is often inevitable. Semaglutide (Sem), a novel GLP-1 analogue, is primarily utilized in managing Type 2 diabetes mellitus (T2DM). Recent research indicates that semaglutide may reduce the risk of major adverse cardiovascular events. Therefore, the purpose of this study is to explore whether semaglutide can ameliorate MIRI and explore its potential mechanism. Methods and results: : A mouse model of myocardial ischemia-reperfusion (I/R) was created by ligating the left anterior descending coronary artery (LAD) first for 45 min and then reperfusing the heart for 24 h. Assessment of cardiac function and fibrosis were conducted through small animal ultrasound and Masson's staining. It was observed that semaglutide enhanced cardiac function recovery and diminished fibrosis in the I/R model. Conclusion: Semaglutide can reduce I/R-induced myocardial injury by inhibiting the ferroptosis of cardiomyocytes. In the mechanism, semaglutide mainly reduce the expression of S100A9 via the activation of PKC signaling pathway. Therefore, semaglutide is considered as a potential treatment option for MIRI.
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