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 StatementsMeSH KeywordsAnti-Arrhythmia AgentsArrhythmias, CardiacHumansMitochondriaMitochondrial DiseasesModels, CardiovascularConceptsMitochondrial 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
2012
GSH or Palmitate Preserves Mitochondrial Energetic/Redox Balance, Preventing Mechanical Dysfunction in Metabolically Challenged Myocytes/Hearts From Type 2 Diabetic Mice
Tocchetti CG, Caceres V, Stanley BA, Xie C, Shi S, Watson WH, O’Rourke B, Spadari-Bratfisch RC, Cortassa S, Akar FG, Paolocci N, Aon MA. GSH or Palmitate Preserves Mitochondrial Energetic/Redox Balance, Preventing Mechanical Dysfunction in Metabolically Challenged Myocytes/Hearts From Type 2 Diabetic Mice. Diabetes 2012, 61: 3094-3105. PMID: 22807033, PMCID: PMC3501888, DOI: 10.2337/db12-0072.Peer-Reviewed Original ResearchConceptsMechanical dysfunctionReactive oxygen speciesType 2 diabetic db/db miceDiabetic db/db miceHigh glucoseType 2 diabetic patientsType 2 diabetic miceDb/db miceLower cardiac performanceLimited exercise capacityPoor glycemic controlType 2 diabetesΒ-agonist isoproterenolCardiac work demandsFatty acid palmitateExercise capacitySympathetic driveGlycemic controlDiabetic patientsDiabetic miceDb miceHeart dysfunctionPatient's inabilityMitochondrial reactive oxygen speciesHeart preparation
2005
Mitochondrial criticality: A new concept at the turning point of life or death
Aon MA, Cortassa S, Akar FG, O'Rourke B. Mitochondrial criticality: A new concept at the turning point of life or death. Biochimica Et Biophysica Acta 2005, 1762: 232-240. PMID: 16242921, PMCID: PMC2692535, DOI: 10.1016/j.bbadis.2005.06.008.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsMeSH KeywordsAnimalsCell DeathElectric ConductivityHumansMitochondriaModels, BiologicalReceptors, GABA-A