2018
The Mitochondrial Translocator Protein and the Emerging Link Between Oxidative Stress and Arrhythmias in the Diabetic Heart
Ilkan Z, Akar FG. The Mitochondrial Translocator Protein and the Emerging Link Between Oxidative Stress and Arrhythmias in the Diabetic Heart. Frontiers In Physiology 2018, 9: 1518. PMID: 30416455, PMCID: PMC6212558, DOI: 10.3389/fphys.2018.01518.Peer-Reviewed Original Research
2017
Oxidative stress and inflammation as central mediators of atrial fibrillation in obesity and diabetes
Karam BS, Chavez-Moreno A, Koh W, Akar JG, Akar FG. Oxidative stress and inflammation as central mediators of atrial fibrillation in obesity and diabetes. Cardiovascular Diabetology 2017, 16: 120. PMID: 28962617, PMCID: PMC5622555, DOI: 10.1186/s12933-017-0604-9.Peer-Reviewed Original ResearchConceptsAtrial fibrillationOxidative stressCommon sustained cardiac arrhythmiaMaintenance of AFSustained cardiac arrhythmiaDiabetic heartElectrical remodelingRisk factorsAtrial excitabilityTherapeutic strategiesCardiac arrhythmiasInflammationCentral mediatorObesityDiabetesFibrillationMechanistic linkMellitusArrhythmiasExcitability
2013
Glutathione 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
2011
Biophysical properties and functional consequences of reactive oxygen species (ROS)‐induced ROS release in intact myocardium
Biary N, Xie C, Kauffman J, Akar FG. Biophysical properties and functional consequences of reactive oxygen species (ROS)‐induced ROS release in intact myocardium. The Journal Of Physiology 2011, 589: 5167-5179. PMID: 21825030, PMCID: PMC3225672, DOI: 10.1113/jphysiol.2011.214239.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntioxidantsArrhythmias, CardiacCyclosporineDiazepamEthidiumFluorescenceFluorescent DyesHydrogen PeroxideIn Vitro TechniquesIntracellular MembranesMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMyocardiumOrganometallic CompoundsOxidantsOxidative StressRatsSalicylatesSuperoxidesVoltage-Dependent Anion ChannelsConceptsIncidence of arrhythmiasIntact myocardiumOxidative stressMitochondrial permeability transition poreReactive oxygen speciesSustained ventricular tachycardiaROS releaseExposure of heartsGlobal oxidative stressPerfusion of heartsSuperoxide dismutase/catalase mimetic EUK-134Functional consequencesOS protocolArrhythmia scoreAcute modelDihydroethidium fluorescenceUntreated heartsVentricular tachycardiaVentricular fibrillationOxygen speciesArrhythmic consequencesElevated ROS levelsRat heartEUK-134PerfusionMitochondria are sources of metabolic sink and arrhythmias
Akar FG, O'Rourke B. Mitochondria are sources of metabolic sink and arrhythmias. Pharmacology & Therapeutics 2011, 131: 287-294. PMID: 21513732, PMCID: PMC3138548, DOI: 10.1016/j.pharmthera.2011.04.005.Peer-Reviewed Original Research
2009
From mitochondrial dynamics to arrhythmias
Aon MA, Cortassa S, Akar FG, Brown DA, Zhou L, O’Rourke B. From mitochondrial dynamics to arrhythmias. The International Journal Of Biochemistry & Cell Biology 2009, 41: 1940-1948. PMID: 19703656, PMCID: PMC2732583, DOI: 10.1016/j.biocel.2009.02.016.Peer-Reviewed Original ResearchConceptsWhole cellsMitochondrial membrane potentialMode of functionMitochondrial networkOxidative stressMitochondrial dynamicsReactive oxygen speciesMitochondrial criticalityMitochondria behaveMitochondriaCellular excitabilityOxygen speciesMembrane potentialPhysiological conditionsROSCatastrophic arrhythmiasCellsCardiac cellsEnergetic failureNormal conditionsSpeciesMessengerNADHStressBroad range
2008
A ligand to the mitochondrial benzodiazepine receptor prevents ventricular arrhythmias and LV dysfunction after ischemia or glutathione depletion
Brown D, Aon M, Akar F, O’Rourke B. A ligand to the mitochondrial benzodiazepine receptor prevents ventricular arrhythmias and LV dysfunction after ischemia or glutathione depletion. The FASEB Journal 2008, 22: 747.7-747.7. DOI: 10.1096/fasebj.22.1_supplement.747.7.Peer-Reviewed Original ResearchContractile dysfunctionBenzodiazepine receptorsGlobal ischemia/reperfusionOxidative stressMitochondrial benzodiazepine receptorIschemia/reperfusionGuinea pig heartsSignificant clinical implicationsAnti-oxidant defensesReduced arrhythmiasLV dysfunctionVentricular dysfunctionR injuryVentricular arrhythmiasInduced arrhythmiasNormoxic perfusionIsolated myocytesDysfunctionClinical implicationsArrhythmiasIntact heartMetabolic challengesPig heartsGlutathione depletionMitochondrial membrane potential
2003
Phenotypic differences in transient outward K+ current of human and canine ventricular myocytes: insights into molecular composition of ventricular Ito
Akar FG, Wu RC, Deschenes I, Armoundas AA, Piacentino V, Houser SR, Tomaselli GF. Phenotypic differences in transient outward K+ current of human and canine ventricular myocytes: insights into molecular composition of ventricular Ito. AJP Heart And Circulatory Physiology 2003, 286: h602-h609. PMID: 14527940, DOI: 10.1152/ajpheart.00673.2003.Peer-Reviewed Original ResearchConceptsTransient outwardPhenotypic differencesKv channel-interacting proteinsIndependent transient outwardChannel-interacting proteinsProtein chemical techniquesSteady-state inactivationCanine ventricular myocytesWestern blot analysisElectrical remodelingChannel subunit genesMonoexponential time coursePharmacological sensitivityVentricular repolarizationCardiac diseaseElectrophysiological roleCanine ventricularHuman cardiac diseasePosttranslational modificationsVentricular myocytesSubunit genePharmacological propertiesDiseased heartPhenotypic propertiesOxidative stress