2016
Reducing mitochondrial bound hexokinase II mediates transition from non-injurious into injurious ischemia/reperfusion of the intact heart
Nederlof R, Gürel-Gurevin E, Eerbeek O, Xie C, Deijs GS, Konkel M, Hu J, Weber NC, Schumacher CA, Baartscheer A, Mik EG, Hollmann MW, Akar FG, Zuurbier CJ. Reducing mitochondrial bound hexokinase II mediates transition from non-injurious into injurious ischemia/reperfusion of the intact heart. Journal Of Physiology And Biochemistry 2016, 73: 323-333. PMID: 28258543, PMCID: PMC5534207, DOI: 10.1007/s13105-017-0555-3.Peer-Reviewed Original ResearchConceptsIschemia/reperfusionR injuryCardiac energeticsRecovery of functionHexokinase IISignificant LDH releasePossible underlying mechanismsIschemic insultCardiac recoveryControl heartsMtHKIIReperfusionIschemiaDHE fluorescenceRat heartR intervalLDH releasePeptide treatmentIntact heartInjuryUnderlying mechanismHeartMVO2NecrosisTreatment
2013
TAT-HKII induced reduction in mitochondrial bound hexokinase II increases ischemia reperfusion injury by increased respiration and increased ROS levels
Nederlof R, Guerel E, Xie C, Eerbeek O, Koeman A, Hollmann M, Southworth R, Akar F, Mik E, Zuurbier C. TAT-HKII induced reduction in mitochondrial bound hexokinase II increases ischemia reperfusion injury by increased respiration and increased ROS levels. European Heart Journal 2013, 34: 3694. DOI: 10.1093/eurheartj/eht309.3694.Peer-Reviewed Original ResearchMitochondrial oxygen tensionPeptide treatmentReperfusion injuryCardiac functionLDH activityROS productionControl groupHexokinase IIIschemia/reperfusion injuryOxygen consumptionIschemia-reperfusion injuryReactive oxygen speciesOxygen tensionCardiac oxygen consumptionCell deathBorderline ischemiaReperfusion necrosisR damageMin reperfusionReversible ischemiaIrreversible ischemiaMin ischemiaIschemiaTreatment groupsReperfusion
2005
The mitochondrial origin of postischemic arrhythmias
Akar FG, Aon MA, Tomaselli GF, O'Rourke B. The mitochondrial origin of postischemic arrhythmias. Journal Of Clinical Investigation 2005, 115: 3527-3535. PMID: 16284648, PMCID: PMC1280968, DOI: 10.1172/jci25371.Peer-Reviewed Original ResearchMeSH KeywordsAction PotentialsAnimalsAnionsArrhythmias, CardiacDose-Response Relationship, DrugElectrophysiologyGuinea PigsHeartIntracellular MembranesIon ChannelsIschemiaMembrane PotentialsMicroscopy, ConfocalMitochondria, HeartMyocardial IschemiaMyocardial ReperfusionMyocardial Reperfusion InjuryMyocardiumMyocytes, CardiacOscillometryReactive Oxygen SpeciesReceptors, GABA-AReperfusion InjuryTemperatureTime FactorsConceptsAction potentialsVentricular fibrillationPostischemic functional recoveryIschemic heart diseaseGuinea pig heartsNew therapeutic targetsAbnormal electrical activationPostischemic arrhythmiasReperfusion arrhythmiasFunctional recoveryGlobal ischemiaHeart diseaseBolus infusionArrhythmia preventionElectrophysiological changesAP shorteningControl heartsPostischemic heartsBenzodiazepine receptorsElectrophysiological substrateTherapeutic targetArrhythmiasReperfusionPig heartsMitochondrial benzodiazepine receptor