title: Inhibition of mitochondrial permeability transition pore opening: translation to patients.
abstract: A large body of experimental evidence indicates that during an acute myocardial infarction (AMI), tissue injury occurring after reperfusion represents a significant amount of the whole, irreversible damage. It is now recognized that mitochondrial permeability transition pore opening plays a crucial role in this specific component of myocardial infarction. Ischaemic postconditioning and cyclosporine A (CsA) have been shown to dramatically reduce infarct size in many animal species. Recent proof-of-concept clinical trials support the idea that lethal myocardial reperfusion injury is also of significant importance in patients with ongoing AMI, and that targeting mitochondrial permeability transition by either percutaneous coronary intervention postconditioning or CsA can reduce infarct size and improve the recovery of contractile function after reperfusion. Large-scale trials are ongoing to address whether these new treatments may improve clinical outcome in reperfused AMI patients.
authors.affiliation: Laboratoire de Physiologie Lyon-Nord, Inserm U 886, 8, Avenue Rockefeller, 69373 Lyon, France.
authors.forename: Ludovic
authors.initials: L
authors.lastname: Gomez
authors.forename: Bo
authors.initials: B
authors.lastname: Li
authors.forename: Nathan
authors.initials: N
authors.lastname: Mewton
authors.forename: Ingrid
authors.initials: I
authors.lastname: Sanchez
authors.forename: Christophe
authors.initials: C
authors.lastname: Piot
authors.forename: Meier
authors.initials: M
authors.lastname: Elbaz
authors.forename: Michel
authors.initials: M
authors.lastname: Ovize
mesh_terms: D015906:Angioplasty, Balloon, Coronary; D000818:Animals; D002316:Cardiotonic Agents / Q000627:therapeutic use*; D016572:Cyclosporine / Q000627:therapeutic use*; D006801:Humans; D008929:Mitochondria, Heart / Q000187:drug effects* / Q000378:metabolism; D033681:Mitochondrial Membrane Transport Proteins / Q000037:antagonists & inhibitors* / Q000378:metabolism; D000083162:Mitochondrial Permeability Transition Pore; D009200:Myocardial Contraction / Q000187:drug effects; D009203:Myocardial Infarction / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D002316:Cardiotonic Agents; D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; D016572:Cyclosporine