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 groupsReperfusionPathophysiological Consequences of TAT-HKII Peptide Administration Are Independent of Impaired Vascular Function and Ensuing Ischemia
Nederlof R, Xie C, Eerbeek O, Koeman A, Milstein DM, Hollmann MW, Mik EG, Warley A, Southworth R, Akar FG, Zuurbier CJ. Pathophysiological Consequences of TAT-HKII Peptide Administration Are Independent of Impaired Vascular Function and Ensuing Ischemia. Circulation Research 2013, 112: e8-e13. PMID: 23329797, PMCID: PMC3596767, DOI: 10.1161/circresaha.112.274308.Peer-Reviewed Original ResearchConceptsVascular functionIschemic preconditioningMyocardial dysfunctionCardiac functionPeptide administrationHexokinase IIOptical action potential mappingAcute myocardial dysfunctionImpaired vascular functionIschemia-reperfusion injuryDeleterious effectsIschemic injuryCardioprotective effectsProtective effectIschemiaPathophysiological consequencesIntact myocardiumDehydrogenase releaseIntact heartAdministrationLactate productionDysfunctionRole of mitochondriaInjuryCritical regulator
2011
07 Mitochondrial hexokinase II is essential for cardiac function and ischaemic preconditioning
Smeele K, Southworth R, Wu R, Xie C, Nederlof R, Warley A, Koeman A, Eerbeek O, Akar F, Ardehali H, Hollmann M, Zuurbier C. 07 Mitochondrial hexokinase II is essential for cardiac function and ischaemic preconditioning. Heart 2011, 97: e8. DOI: 10.1136/heartjnl-2011-301156.7.Peer-Reviewed Original ResearchIschemic preconditioningCardiac functionWT heartsProtective effectBaseline cardiac functionNormal cardiac functionMitochondrial permeability transition openingContractile impairmentIR injuryReperfusion injuryAcute reductionMyocardial functionGlycolytic enzymes hexokinaseMitochondrial hexokinase-IIEx vivoCardiac contractionMild mitochondrial uncouplingMitochondrial membrane depolarisationMembrane depolarisationHexokinase IIHKIIHeartMitochondrial swellingTissue disruptionInjury