2022
Atrial AMP-activated protein kinase is critical for prevention of dysregulation of electrical excitability and atrial fibrillation
Su KN, Ma Y, Cacheux M, Ilkan Z, Raad N, Muller GK, Wu X, Guerrera N, Thorn SL, Sinusas AJ, Foretz M, Viollet B, Akar JG, Akar FG, Young LH. Atrial AMP-activated protein kinase is critical for prevention of dysregulation of electrical excitability and atrial fibrillation. JCI Insight 2022, 7: e141213. PMID: 35451373, PMCID: PMC9089788, DOI: 10.1172/jci.insight.141213.Peer-Reviewed Original ResearchMeSH KeywordsAMP-Activated Protein KinasesAnimalsAtrial FibrillationAtrial RemodelingConnexinsIon ChannelsMiceMyocytes, CardiacTranscription FactorsConceptsTranscription factorsKey transcription factorMaster metabolic regulatorIon channel subunitsGap junction proteinTranscriptional reprogrammingAMPK deletionProtein kinaseBiological functionsTranscriptional downregulationMetabolic regulatorChannel subunitsIon channelsAMPK expressionMetabolic stressAtrial fibrillationAMPKJunction proteinsElectrical excitabilityHomeostatic roleStructural remodelingConnexinsAtrial ion channelsRemodelingDownregulation
2009
In Vivo Assessment of Myocardial Glucose Uptake by Positron Emission Tomography in Adults With the PRKAG2 Cardiac Syndrome
Ha AC, Renaud JM, deKemp RA, Thorn S, DaSilva J, Garrard L, Yoshinaga K, Abraham A, Green MS, Beanlands RS, Gollob MH. In Vivo Assessment of Myocardial Glucose Uptake by Positron Emission Tomography in Adults With the PRKAG2 Cardiac Syndrome. Circulation Cardiovascular Imaging 2009, 2: 485-491. PMID: 19920047, DOI: 10.1161/circimaging.109.853291.Peer-Reviewed Original ResearchMeSH KeywordsAdultAMP-Activated Protein KinasesCase-Control StudiesEchocardiographyFemaleFluorodeoxyglucose F18Heart DiseasesHumansMaleMetabolic DiseasesMiddle AgedMutationMyocardiumPhenotypeRadiographic Image Interpretation, Computer-AssistedRubidium RadioisotopesStatistics, NonparametricSyndromeTomography, Emission-ComputedConceptsMyocardial glucose uptakeSignificant myocardial scarFDG-PET imagingPRKAG2 cardiac syndromeCardiac syndromeGlucose uptakeAdult patientsMyocardial scarMetabolic diseasesControl groupMedian blood glucoseEuglycemic hyperinsulinemic clampStable blood glucose levelsBlood glucose levelsInherited metabolic diseaseMin/Positron emission tomography (PET) imagingEmission Tomography ImagingPositron emission tomographyMyocardial glucose transportPerfusion scanBlood glucoseControl subjectsHyperinsulinemic clampAffected patientsDistinct Early Signaling Events Resulting From the Expression of the PRKAG2 R302Q Mutant of AMPK Contribute to Increased Myocardial Glycogen
Folmes KD, Chan AY, Koonen DP, Pulinilkunnil TC, Baczkó I, Hunter BE, Thorn S, Allard MF, Roberts R, Gollob MH, Light PE, Dyck JR. Distinct Early Signaling Events Resulting From the Expression of the PRKAG2 R302Q Mutant of AMPK Contribute to Increased Myocardial Glycogen. Circulation Genomic And Precision Medicine 2009, 2: 457-466. PMID: 20031621, DOI: 10.1161/circgenetics.108.834564.Peer-Reviewed Original ResearchConceptsTransgenic miceR302Q mutationGlycogen contentAcute expressionCardiomyocyte-restricted expressionAMPK activationTransgenic adult miceNeonatal rat cardiomyocytesChronic modelWolff-ParkinsonGlycogen synthase activityWhite syndromeCardiac hypertrophyAdult miceGlycogen storage cardiomyopathyMyocardial glycogenDirect effectCompensatory alterationsRat cardiomyocytesFamilial formsMiceEarly signaling eventCardiomyopathyAMPK activityHeart