2009
Cardiac macrophage migration inhibitory factor inhibits JNK pathway activation and injury during ischemia/reperfusion
Qi D, Hu X, Wu X, Merk M, Leng L, Bucala R, Young LH. Cardiac macrophage migration inhibitory factor inhibits JNK pathway activation and injury during ischemia/reperfusion. Journal Of Clinical Investigation 2009, 119: 3807-3816. PMID: 19920350, PMCID: PMC2786800, DOI: 10.1172/jci39738.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell LineEnzyme ActivationHumansIn Vitro TechniquesIntramolecular OxidoreductasesJNK Mitogen-Activated Protein KinasesMacrophage Migration-Inhibitory FactorsMAP Kinase Kinase 4MiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutMyocardial ContractionMyocardial Reperfusion InjuryMyocardiumReceptors, ImmunologicSignal TransductionConceptsMacrophage migration inhibitory factorIschemia/reperfusionMIF deficiencyCardiac injuryMIF allelesJNK pathway activationRole of MIFRecombinant macrophage migration inhibitory factorExperimental ischemia/reperfusionLow-expression MIF allelePathway activationGreater contractile dysfunctionMIF-/- miceMigration inhibitory factorJNK activationReperfusion injuryContractile dysfunctionCoronary occlusionProinflammatory cytokinesWT heartsReperfusionCell death (BAD) phosphorylationInjuryClinical implicationsInhibitory factor
2006
Activation of AMPK α- and γ-isoform complexes in the intact ischemic rat heart
Li J, Coven DL, Miller EJ, Hu X, Young ME, Carling D, Sinusas AJ, Young LH. Activation of AMPK α- and γ-isoform complexes in the intact ischemic rat heart. AJP Heart And Circulatory Physiology 2006, 291: h1927-h1934. PMID: 16648175, DOI: 10.1152/ajpheart.00251.2006.Peer-Reviewed Original ResearchConceptsAMPK activityAMPK complexAlpha subunit activationDifferent subunit isoformsSerine-threonine kinaseCellular metabolic processesGamma subunit isoformsRegulatory betaAlpha-subunit contentHeterotrimeric complexProtein kinaseAMPK αMultiple isoformsKinase activitySubunit isoformsMetabolic processesAMPK phosphorylationAMPKIsoformsPhysiological regulationKinaseMutationsComplexesKey rolePathophysiological importance
2004
Cardiac myocyte‐specific HIF‐1α deletion alters vascularization, energy availability, calcium flux, and contractility in the normoxic heart
Huang Y, Hickey RP, Yeh JL, Liu D, Dadak A, Young LH, Johnson RS, Giordano FJ. Cardiac myocyte‐specific HIF‐1α deletion alters vascularization, energy availability, calcium flux, and contractility in the normoxic heart. The FASEB Journal 2004, 18: 1138-1140. PMID: 15132980, DOI: 10.1096/fj.04-1510fje.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCalcium SignalingCoronary CirculationDNA-Binding ProteinsEnergy MetabolismGene DeletionGene Expression RegulationHeart Function TestsHypoxia-Inducible Factor 1Hypoxia-Inducible Factor 1, alpha SubunitMiceMice, Inbred C57BLMice, KnockoutMyocardial ContractionMyocardiumMyocytes, CardiacNeovascularization, PhysiologicNuclear ProteinsOxygen ConsumptionReverse Transcriptase Polymerase Chain ReactionRNA, MessengerTranscription FactorsTranscription, GeneticConceptsCardiac functionCalcium fluxHypoxia-inducible transcription factor HIF-1alphaCardiac oxygen deliveryDisease statesHIF-1alphaSkeletal muscleCardiac contractile dysfunctionHigh-energy phosphate contentCardiovascular disease statesResting pulse rateTranscription factor HIF-1alphaCoronary vasodilatationMyocardial demandContractile dysfunctionMyocardial hibernationNormoxic heartsOxygen supplyGene expressionCalcium handlingOxygen deliveryPulse rateHeart muscleCardiac muscleMolecular pathology
2003
Insulin resistance and the effects of thiazolidinediones on cardiac metabolism
Young LH. Insulin resistance and the effects of thiazolidinediones on cardiac metabolism. The American Journal Of Medicine 2003, 115: 75-80. PMID: 14678870, DOI: 10.1016/j.amjmed.2003.09.013.BooksMeSH KeywordsAnimalsBlood GlucoseCardiomyopathiesDiabetes Mellitus, Type 2Fatty Acids, NonesterifiedHumansInsulin ResistanceMyocardial ContractionMyocardiumThiazolidinedionesConceptsMyocardial metabolismFree fatty acidsAdministration of thiazolidinedionesImproved glucose metabolismEffects of thiazolidinedionesInsulin-sensitizing effectsRecovery of functionCardiac contractile activityPotential beneficial effectsPostischemic periodDiabetes mellitusMyocardial injuryFFA metabolismInsulin resistanceFatty acid concentrationsContractile activityGlucose metabolismAnimal studiesCardiac metabolismPharmacologic manipulationThiazolidinedionesBeneficial effectsSkeletal muscleHigh rateMetabolism
1990
Metabolic and functional effects of perfluorocarbon distal perfusion during coronary angioplasty
Young L, Jaffe C, Revkin J, McNulty P, Cleman M. Metabolic and functional effects of perfluorocarbon distal perfusion during coronary angioplasty. The American Journal Of Cardiology 1990, 65: 986-990. PMID: 2327360, DOI: 10.1016/0002-9149(90)91001-m.Peer-Reviewed Original ResearchConceptsGreat cardiac veinDistal perfusionLactate releaseEjection fractionVentricular functionCardiac veinBalloon inflationLeft ventricular ejection fractionDistal coronary perfusionMyocardial lactate metabolismVentricular ejection fractionMyocardial lactate releaseRegional contractile functionNet lactate extractionNet lactate releaseCoronary angioplastyLeft anteriorCoronary perfusionLactate extractionContractile functionPerfusionAngioplastyLactate concentrationLactate metabolismOxygenated perfluorocarbon