Cardioprotective Effects of Exenatide In Patients with ST-segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention; Results of Exenatide Myocardial Protection in Revascularization (EMPIRE) Study

Rationale, design, and baseline characteristics in Evaluation of LIXisenatide in Acute Coronary Syndrome, a long-term cardiovascular end point trial of lixisenatide versus placebo

“…In small placebo-controlled studies, GLP-1RA treatment improved myocardial salvage and reduced infarct size. 43,44 A larger retrospective analysis revealed that the nonrandomized use of GLP-1RA was associated with a 19% lower CV event risk compared with other glucose-lowering agents. 45 In addition, a metaanalysis revealed a significant reduction in CV events among individuals taking GLP-1RAs rather than placebo or other glucose-lowering agents.…”

Protein kinase Cβ mediates downregulated expression of glucagon-like peptide-1 receptor in hypertensive rat renal arteries

“…Clinical and experimental evidence suggest that GLP-1 and related agents exert cardiovascular protection through GLP-1R in myocardial infarction, diabetes, and Exendin-4 (log mol/l) Exendin-4 (nmol/l) Phe hypertension [11,17,23,24]. The major findings of this study include the relaxations to exendin-4 were endothelium dependent in WKY renal arteries; exendin-4 induced significantly less relaxations in SHR arteries and the relaxations in WKY arteries were antagonized by selective GLP-1R antagonist, exendin 9-39; the impaired relaxations to exendin-4 in SHR arteries were restored by treatment with inhibitors of PKC and PKCb; the reduced GLP-1R expression in SHR arteries was increased by treatment with inhibitors of PKC and PKCb; the PKCb level was elevated in renal arteries from SHR compared with WKY; and PKC-activating agent PMA induced the impairment of exendin-4-induced relaxation and the reduction of the GLP-1R expression in WKY arteries, which were reversed by treatment with inhibitors of PKC and PKCb.…”

The NHLBI-Sponsored Consortium for preclinicAl assESsment of cARdioprotective Therapies (CAESAR)

“…Over the past 40 years, innumerable therapies have been claimed to be efficacious in limiting the size of a myocardial infarction in animal models 5 ; based upon these “positive” preclinical data, many of these interventions have been tried in patients but the results have been disappointing. Although several agents including metoprolol 6 , cyclosporine 7, 8 , ANP 9 , and exenatide 10 show promise in early clinical trials, to date, there is no accepted method to reduce infarct size in the clinical arena beyond timely reperfusion 5 .…”