2020
NLRX1 Deletion Increases Ischemia-Reperfusion Damage and Activates Glucose Metabolism in Mouse Heart
Zhang H, Xiao Y, Nederlof R, Bakker D, Zhang P, Girardin SE, Hollmann MW, Weber NC, Houten SM, van Weeghel M, Kibbey RG, Zuurbier CJ. NLRX1 Deletion Increases Ischemia-Reperfusion Damage and Activates Glucose Metabolism in Mouse Heart. Frontiers In Immunology 2020, 11: 591815. PMID: 33362773, PMCID: PMC7759503, DOI: 10.3389/fimmu.2020.591815.Peer-Reviewed Original ResearchConceptsIschemia-reperfusion injuryNOD-like receptorsMouse heartsKO heartsGlucose metabolismCardiac ischemia-reperfusion injuryIschemia-reperfusion damageMin of reperfusionCardiac IR injurySurvival pathwaysPro-inflammatory memberCardiac glucose metabolismInnate immune systemCardiac oxygen consumptionFatty acid oxidationInflammatory parametersPyruvate dehydrogenase fluxIR injuryEarly reperfusionInflammatory mediatorsMin reperfusionSevere ischemiaC-palmitateImmune systemReperfusion
2018
Cardiac metabolic effects of KNa1.2 channel deletion and evidence for its mitochondrial localization
Smith CO, Wang YT, Nadtochiy SM, Miller JH, Jonas EA, Dirksen RT, Nehrke K, Brookes PS. Cardiac metabolic effects of KNa1.2 channel deletion and evidence for its mitochondrial localization. The FASEB Journal 2018, 32: 6135-6149. PMID: 29863912, PMCID: PMC6181635, DOI: 10.1096/fj.201800139r.Peer-Reviewed Original ResearchCardiac metabolic effectsMetabolic effectsChannel deletionCardiac ischemia-reperfusion injuryIschemia-reperfusion injuryWild-type miceCardiac metabolomeBaseline differencesBody fatVolatile anestheticsElectrophysiological evidenceMiceKCNT2Physiological roleCardiomyocytesFatMembrane preparationsMolecular identityCardioprotectionEvidenceInjuryMitochondrial localizationAnesthetics
2012
miR-1 Exacerbates Cardiac Ischemia-Reperfusion Injury in Mouse Models
Pan Z, Sun X, Ren J, Li X, Gao X, Lu C, Zhang Y, Sun H, Wang Y, Wang H, Wang J, Xie L, Lu Y, Yang B. miR-1 Exacerbates Cardiac Ischemia-Reperfusion Injury in Mouse Models. PLOS ONE 2012, 7: e50515. PMID: 23226300, PMCID: PMC3511560, DOI: 10.1371/journal.pone.0050515.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBase SequenceCaspase 3Chaperonin 60Creatine KinaseDisease Models, AnimalGene Expression RegulationGene Knockdown TechniquesHumansL-Lactate DehydrogenaseMaleMiceMice, Inbred C57BLMice, TransgenicMicroRNAsMyocardial InfarctionMyocardial IschemiaMyocytes, CardiacOligonucleotidesProtein Kinase C-epsilonReperfusion InjuryConceptsMiR-1MiR-1 Tg miceNucleic acid-modified oligonucleotidesEffects of miR-1Cardiac injuryMiR-1 knockdownCardiac ischemia/reperfusion injuryMiR-1 expressionRegulation of miR-1Ischemia/reperfusion injuryMiR-1 levelsModified oligonucleotidesAttenuated cardiac ischemia/reperfusion injuryRegulating cardiac injuryCardiac ischemia-reperfusion injuryCardiac infarction areaSolid in vivo evidenceIschemia-reperfusion injuryPotential therapeutic advantageProtein kinase C epsilonCaspase-3 expressionHeat shock protein 60Luciferase assayCardiac myocytesTreated mice
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