2024
Quantitative Assessment of Mitochondrial Morphology and Electrophysiological Function in the Diabetic Heart
Cacheux M, Rudokas M, Tieu A, Rizk J, Hummel M, Akar F. Quantitative Assessment of Mitochondrial Morphology and Electrophysiological Function in the Diabetic Heart. Methods In Molecular Biology 2024, 2803: 75-86. PMID: 38676886, DOI: 10.1007/978-1-0716-3846-0_6.Peer-Reviewed Original ResearchConceptsMitochondrial shapeMitochondrial networkMitochondrial architectureSubcellular localizationMitochondrial morphologyDiabetic heartOxidative phosphorylationATP synthesisAction potentialsSarcolemmal ion channelsExcitation-contraction couplingFission eventsOptical action potentialsExcitation-contractionCardiac myocytesElectrophysiological properties
2015
The Mitochondrial Translocator Protein and Arrhythmogenesis in Ischemic Heart Disease
Motloch LJ, Hu J, Akar FG. The Mitochondrial Translocator Protein and Arrhythmogenesis in Ischemic Heart Disease. Oxidative Medicine And Cellular Longevity 2015, 2015: 234104. PMID: 25918579, PMCID: PMC4397036, DOI: 10.1155/2015/234104.Peer-Reviewed Original ResearchConceptsIschemic heart diseaseHeart diseaseTranslocator proteinAcute ischemia-reperfusion injuryReactive oxygen speciesIschemia-reperfusion injuryMultiple organ systemsExcitation-contraction couplingMultiple cardiovascular disordersPermeability transition poreRole of TSPOMyocardial infarctionInflammatory processDiverse pathophysiological processesImmune responseCardiovascular disordersTherapeutic targetPathophysiological processesOrgan systemsDiagnostic markerMitochondrial dysfunctionDiseaseAbundant expressionMitochondrial translocator proteinROS release
2013
Mitochondrial targets for arrhythmia suppression: is there a role for pharmacological intervention?
Akar FG. Mitochondrial targets for arrhythmia suppression: is there a role for pharmacological intervention? Journal Of Interventional Cardiac Electrophysiology 2013, 37: 249-258. PMID: 23824789, DOI: 10.1007/s10840-013-9809-3.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsMitochondrial targetsMitochondrial dysfunctionCritical cellular functionsCell death pathwaysCellular redox statusIon channel functionMitochondrial networkCellular functionsDeath pathwaysMitochondrial originIschemia-reperfusion injuryCommon cardiovascular disordersMitochondrial bioenergeticsExcitation-contraction couplingChannel functionRedox statusMechanistic linkHeart failureArrhythmia suppressionPharmacological interventionsCardiovascular disordersCentral mechanismsDysfunctionArrhythmogenesisEnergy production
2008
Effects of 4′-chlorodiazepam on cellular excitation–contraction coupling and ischaemia–reperfusion injury in rabbit heart
Brown DA, Aon MA, Akar FG, Liu T, Sorarrain N, O’Rourke B. Effects of 4′-chlorodiazepam on cellular excitation–contraction coupling and ischaemia–reperfusion injury in rabbit heart. Cardiovascular Research 2008, 79: 141-149. PMID: 18304929, PMCID: PMC2562874, DOI: 10.1093/cvr/cvn053.Peer-Reviewed Original ResearchConceptsIschaemia-reperfusion injuryExcitation-contraction couplingReperfusion arrhythmiasRabbit heartsDose-dependent negative inotropic responseCellular excitation-contraction couplingPost-ischemic cardiac dysfunctionOnset of reperfusionMin of reperfusionSingle bolus doseNegative inotropic responseIschaemia/reperfusionIntracellular calcium transientsSarcolemmal ion channelsIsolated rabbit cardiomyocytesIon channelsCardiac action potentialContractile impairmentCardiac dysfunctionBolus doseContractile dysfunctionInotropic responseGlobal ischaemiaVoltage clamp methodCalcium current