title: Optimising cardioprotection during myocardial ischaemia: targeting potential intracellular pathways with glucagon-like peptide-1.
abstract: Coronary heart disease and type-2 diabetes are both major global health burdens associated with an increased risk of myocardial infarction (MI). Following MI, ischaemia-reperfusion injury (IRI) remains a significant contributor to myocardial injury at the cellular level. Research has focussed on identifying a strategy or intervention to minimise IRI to optimise reperfusion therapy, with the aim of delivering a superior clinical outcome. The incretin hormone glucagon-like peptide-1, already an established basis for the treatment of type-2 diabetes, also has the potential to protect against IRI. We explain the physiology and cellular processes involved in IRI, and the intracellular pathways activated by GLP-1, which could intercept IRI and deliver cardioprotection. The review also examines the current preclinical and clinical evidence for GLP-1 in cardioprotection and future directions for research as we look for an effective adjunctive treatment to minimise IRI.
authors.forename: Sophie J
authors.initials: SJ
authors.lastname: Clarke
authors.forename: Liam M
authors.initials: LM
authors.lastname: McCormick
authors.affiliation: Department of Cardiovascular Medicine, University of Cambridge, Addenbrooke's Hospital, Cambridge, UK. dpd24@medschl.cam.ac.uk.
authors.forename: David P
authors.initials: DP
authors.lastname: Dutka
mesh_terms: D000818:Animals; D002316:Cardiotonic Agents / Q000008:administration & dosage*; D016503:Drug Delivery Systems / Q000379:methods*; D052216:Glucagon-Like Peptide 1 / Q000008:administration & dosage*; D006801:Humans; D007424:Intracellular Fluid / Q000187:drug effects / Q000378:metabolism*; D017202:Myocardial Ischemia / Q000378:metabolism* / Q000473:pathology / Q000517:prevention & control*; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology
chemical_list: D002316:Cardiotonic Agents; D052216:Glucagon-Like Peptide 1