2020
Feasibility study of PET dynamic imaging of [18F]DHMT for quantification of reactive oxygen species in the myocardium of large animals
Wu J, Boutagy NE, Cai Z, Lin SF, Zheng MQ, Feher A, Stendahl JC, Kapinos M, Gallezot JD, Liu H, Mulnix T, Zhang W, Lindemann M, Teng JK, Miller EJ, Huang Y, Carson RE, Sinusas AJ, Liu C. Feasibility study of PET dynamic imaging of [18F]DHMT for quantification of reactive oxygen species in the myocardium of large animals. Journal Of Nuclear Cardiology 2020, 29: 216-225. PMID: 32415628, PMCID: PMC7666654, DOI: 10.1007/s12350-020-02184-3.Peer-Reviewed Original ResearchAnimalsDogsFeasibility StudiesHumansMyocardiumPositron-Emission TomographyReactive Oxygen SpeciesSuperoxides
2016
Mitochondrial Reactive Oxygen Species Mediate Cardiac Structural, Functional, and Mitochondrial Consequences of Diet‐Induced Metabolic Heart Disease
Sverdlov AL, Elezaby A, Qin F, Behring JB, Luptak I, Calamaras TD, Siwik DA, Miller EJ, Liesa M, Shirihai OS, Pimentel DR, Cohen RA, Bachschmid MM, Colucci WS. Mitochondrial Reactive Oxygen Species Mediate Cardiac Structural, Functional, and Mitochondrial Consequences of Diet‐Induced Metabolic Heart Disease. Journal Of The American Heart Association 2016, 5: e002555. PMID: 26755553, PMCID: PMC4859372, DOI: 10.1161/jaha.115.002555.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine TriphosphateAnimalsCatalaseDiet, High-FatDietary SucroseDisease Models, AnimalElectron Transport Complex IElectron Transport Complex IIEnergy MetabolismHypertrophy, Left VentricularMice, Inbred C57BLMice, TransgenicMitochondria, HeartMitochondrial DiseasesMutationOxidation-ReductionOxidative StressProtein Processing, Post-TranslationalReactive Oxygen SpeciesVentricular Dysfunction, LeftVentricular Function, LeftConceptsOxidative posttranslational modificationsMitochondrial reactive oxygen speciesPosttranslational modificationsReactive oxygen speciesMetabolic heart diseaseATP synthesisMitochondrial dysfunctionCardiac mitochondrial proteinsSite-directed mutationsMitochondrial proteinsTransgenic miceWild-type miceComplex IMitochondriaMitochondrial abnormalitiesHigh palmitateOxygen speciesCardiac mitochondriaCys100Mitochondrial consequencesCys103Key mediatorProteinH2O2 productionHigh-fat high-sucrose diet
2014
High fat, high sucrose diet causes cardiac mitochondrial dysfunction due in part to oxidative post-translational modification of mitochondrial complex II
Sverdlov AL, Elezaby A, Behring JB, Bachschmid MM, Luptak I, Tu VH, Siwik DA, Miller EJ, Liesa M, Shirihai OS, Pimentel DR, Cohen RA, Colucci WS. High fat, high sucrose diet causes cardiac mitochondrial dysfunction due in part to oxidative post-translational modification of mitochondrial complex II. Journal Of Molecular And Cellular Cardiology 2014, 78: 165-173. PMID: 25109264, PMCID: PMC4268348, DOI: 10.1016/j.yjmcc.2014.07.018.Peer-Reviewed Original ResearchConceptsCysteine oxidative post-translational modificationsOxidative post-translational modificationsCardiac mitochondrial proteinsPost-translational modificationsMetabolic heart diseaseMitochondrial proteinsATP synthesisMitochondrial dysfunctionBasic Mitochondrial BiologyCardiac mitochondriaMitochondrial biologyOxidative stressTag labelingCardiac mitochondrial dysfunctionBiotin switchSubunit AATP productionMitochondrial ROSGSH/GSSG ratioFunctional consequencesMitochondriaReversible oxidationGSSG ratioProteinSDHA