Glucagon-Like Peptide-1
Autor: | Stephen P. Hoole, Joel P. Giblett, David P. Dutka, Sophie J. Clarke |
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Rok vydání: | 2016 |
Předmět: |
0301 basic medicine
lcsh:Diseases of the circulatory (Cardiovascular) system medicine.medical_specialty ATP adenosine triphosphate IC ischemic conditioning medicine.medical_treatment DPP dipeptidyl-peptidase IR ischemia reperfusion 030204 cardiovascular system & hematology STATE-OF-THE-ART REVIEW 03 medical and health sciences 0302 clinical medicine Internal medicine medicine Cardioprotective Agent GLP-1 glucagon-like peptide 1-(7-36) amide Myocardial infarction ANP atrial natriuretic peptide Cardioprotection ischemia reperfusion injury Myocardial stunning PCI percutaneous coronary intervention business.industry GLP-1RA GLP-1 receptor agonist RISK reperfusion injury survival kinase Insulin percutaneous coronary intervention Percutaneous coronary intervention STEMI ST-segment elevation myocardial infarction medicine.disease Glucagon-like peptide-1 ischemic heart disease AMI acute myocardial infarction SAFE survivor-activating factor enhancement GLP-1R GLP-1 receptor 030104 developmental biology glucagon-like peptide-1 lcsh:RC666-701 Cardiology Ischemic preconditioning Cardiology and Cardiovascular Medicine business GLP-1 |
Zdroj: | JACC: Basic to Translational Science JACC: Basic to Translational Science, Vol 1, Iss 4, Pp 267-276 (2016) |
ISSN: | 2452-302X |
DOI: | 10.1016/j.jacbts.2016.03.011 |
Popis: | Summary Glucagon-like peptide-1-(7-36) amide (GLP-1) is a human incretin hormone responsible for the release of insulin in response to food. Pre-clinical and human physiological studies have demonstrated cardioprotection from ischemia-reperfusion injury. It can reduce infarct size, ischemic left ventricular dysfunction, and myocardial stunning. GLP-1 receptor agonists have also been shown to reduce infarct size in myocardial infarction. The mechanism through which this protection occurs is uncertain but may include hijacking the subcellular pathways of ischemic preconditioning, modulation of myocardial metabolism, and hemodynamic effects including peripheral, pulmonary, and coronary vasodilatation. This review will assess the evidence for each of these mechanisms in turn. Challenges remain in successfully translating cardioprotective interventions from bench-to-bedside. The window of cardioprotection is short and timing of cardioprotection in the appropriate clinical setting is critically important. We will emphasize the need for high-quality, well-designed research to evaluate GLP-1 as a cardioprotective agent for use in real-world practice. |
Databáze: | OpenAIRE |
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