Liu Hong. Research Progress of GLP-1 Receptor Agonists in Mitigating Myocardial Ischemia-Reperfusion Injury. 2026. biomedRxiv.202605.00028
Research Progress of GLP-1 Receptor Agonists in Mitigating Myocardial Ischemia-Reperfusion Injury
Corresponding author: Liu Hong, daliliuhong@163.com
DOI: 10.12201/bmr.202605.00028
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Abstract: Glucagon-like peptide-1 receptor agonists (GLP-1RAs) are glucose-lowering agents widely used in the management of type 2 diabetes mellitus. Recent large-scale cardiovascular outcome trials have demonstrated their significant cardioprotective effects. Myocardial ischemia-reperfusion injury (MI/RI) represents a major determinant of adverse prognosis in patients with acute myocardial infarction (AMI) despite successful revascularization, with reperfusion-induced myocardial damage accounting for up to 40%-50% of the final infarct size. This review systematically summarizes the protective effects of GLP-1RAs against MI/RI and their underlying mechanisms, integrating evidence across multiple dimensions including receptor-mediated signal transduction, oxidative stress modulation, calcium homeostasis, inflammatory response suppression, mitochondrial function preservation, and regulation of programmed cell death. The preclinical and clinical advances of representative GLP-1RAs are also discussed. Furthermore, current challenges in clinical translation are analyzed and future research directions are proposed, aiming to provide a theoretical foundation for the adjunctive use of GLP-1RAs in AMI reperfusion therapy.Keywords: Myocardial Reperfusion Injury; Glucagon-Like Peptide-1 Receptor Agonists; Acute Myocardial Infarction; Myocardial Protection; Cell Death
Key words: Myocardial Reperfusion Injury; Glucagon-Like Peptide-1 Receptor Agonists; Acute Myocardial Infarction; Myocardial Protection; Cell DeathSubmit time: 5 May 2026
Copyright: The copyright holder for this preprint is the author/funder, who has granted biomedRxiv a license to display the preprint in perpetuity. -
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ID Submit time Number Download 1 2026-04-08 10.12201/bmr.202605.00028V1
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