Glucagon-Like Peptide-1

Autor: Stephen P. Hoole, Joel P. Giblett, David P. Dutka, Sophie J. Clarke
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