title: Glucagon-like peptide 1 and cardiac cell survival.
abstract: During myocardial infarction (MI), a variety of mechanisms contribute to activation of cell death processes in cardiomyocytes, which determines the final MI size, subsequent mortality, and post-MI remodeling. The deleterious mechanisms activated during the ischemia and reperfusion phases in MI include oxygen deprival, decreased availability of nutrients and survival factors, accumulation of waste products, generation of oxygen free radicals, calcium overload, neutrophil infiltration in the ischemic area, depletion of energy stores, and opening of the mitochondrial permeability transition pore, all of them contributing to activation of apoptosis and necrosis in cardiomyocytes. Glucagon-like peptide-1 [GLP-1 (7-36) amide] has gained relevance in recent years for metabolic treatment of patients with type 2 diabetes mellitus. Cytoprotection of different cell types, including cardiomyocytes, is among the pleiotropic actions reported for GLP-1. This paper reviews the most relevant experimental studies that have contributed to a better understanding of the molecular mechanisms and intracellular pathways involved in cardioprotection induced by GLP-1 and analyzes in depth its potential role as a therapeutic target both in the ischemic and reperfused myocardium and in other conditions that are associated with myocardial remodeling and heart failure.
authors.affiliation: Área de Ciencias Cardiovasculares, Centro para la Investigación Médica Aplicada, Universidad de Navarra, Pamplona, España. sravassa@unav.es
authors.forename: Susana
authors.initials: S
authors.lastname: Ravassa
authors.forename: Amaia
authors.initials: A
authors.lastname: Zudaire
authors.forename: Javier
authors.initials: J
authors.lastname: Díez
mesh_terms: D000818:Animals; D002316:Cardiotonic Agents / Q000627:therapeutic use*; D002470:Cell Survival; D002478:Cells, Cultured / Q000187:drug effects / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy / Q000378:metabolism; D018819:Dipeptidyl Peptidase 4 / Q000172:deficiency / Q000502:physiology; D054873:Dipeptidyl-Peptidase IV Inhibitors / Q000627:therapeutic use; D004353:Drug Evaluation, Preclinical; D019858:Enteroendocrine Cells / Q000378:metabolism; D004789:Enzyme Activation; D052216:Glucagon-Like Peptide 1 / Q000502:physiology* / Q000627:therapeutic use; D006333:Heart Failure / Q000188:drug therapy / Q000378:metabolism; D006334:Heart Function Tests; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D017202:Myocardial Ischemia / Q000378:metabolism* / Q000473:pathology; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control; D032383:Myocytes, Cardiac / Q000378:metabolism* / Q000473:pathology; D010446:Peptide Fragments / Q000627:therapeutic use; D011494:Protein Kinases / Q000502:physiology; D015398:Signal Transduction
chemical_list: D002316:Cardiotonic Agents; D054873:Dipeptidyl-Peptidase IV Inhibitors; D007004:Hypoglycemic Agents; D010446:Peptide Fragments; C055453:glucagon-like peptide 1 (7-36)amide; D052216:Glucagon-Like Peptide 1; D011494:Protein Kinases; D018819:Dipeptidyl Peptidase 4