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 groupsReperfusionGlutathione oxidation unmasks proarrhythmic vulnerability of chronically hyperglycemic guinea pigs
Xie C, Biary N, Tocchetti CG, Aon MA, Paolocci N, Kauffman J, Akar FG. Glutathione oxidation unmasks proarrhythmic vulnerability of chronically hyperglycemic guinea pigs. AJP Heart And Circulatory Physiology 2013, 304: h916-h926. PMID: 23376824, PMCID: PMC3625895, DOI: 10.1152/ajpheart.00026.2012.Peer-Reviewed Original ResearchConceptsSham-operated heartsChronic hyperglycemiaOxidative stressAPD heterogeneityGuinea pigsOptical action potential mappingType 1 diabetes mellitusVT/VFGuinea pig modelAction potential durationDaily insulinDiabetes mellitusArrhythmia suppressionProarrhythmic propertiesGlycemic levelsVentricular tachycardiaSaline injectionVentricular fibrillationSudden deathGlucose levelsStreptozotocinArrhythmic triggersNormal heartsTreatment groupsPotential duration