2024
Therapeutic Inhibition of LincRNA-p21 Protects Against Cardiac Hypertrophy
Wang Y, Zhang M, Wang R, Lin J, Ma Q, Guo H, Huang H, Liang Z, Cao Y, Zhang X, Lu Y, Liu J, Xiao F, Yan H, Dimitrova N, Huang Z, Mably J, Pu W, Wang D. Therapeutic Inhibition of LincRNA-p21 Protects Against Cardiac Hypertrophy. Circulation Research 2024, 135: 434-449. PMID: 38864216, PMCID: PMC11257812, DOI: 10.1161/circresaha.123.323356.Peer-Reviewed Original ResearchCardiac hypertrophyHeart failureGenome-wide transcriptome analysisCardiac functionDeterioration of cardiac functionResponse to pressure overloadAssociated heart failureTherapeutic potentialLoss-of-function miceDilated cardiomyopathy patientsPressure-overload conditionsInhibit cardiac hypertrophyTranscriptome analysisCardiac-specific knockoutMaladaptive cardiac remodelingLong noncoding RNAsVentricular wall thickeningNoncoding RNAsTranscriptional network analysisCardiomyopathy patientsMarker elevationPressure overloadCardiac remodelingPathological hypertrophyAdverse remodelingStromal Cell-SLIT3/Cardiomyocyte-ROBO1 Axis Regulates Pressure Overload-Induced Cardiac Hypertrophy
Liu X, Li B, Wang S, Zhang E, Schultz M, Touma M, Da Rocha A, Evans S, Eichmann A, Herron T, Chen R, Xiong D, Jaworski A, Weiss S, Si M. Stromal Cell-SLIT3/Cardiomyocyte-ROBO1 Axis Regulates Pressure Overload-Induced Cardiac Hypertrophy. Circulation Research 2024, 134: 913-930. PMID: 38414132, PMCID: PMC10977056, DOI: 10.1161/circresaha.122.321292.Peer-Reviewed Original ResearchConceptsTransverse aortic constrictionAortic constrictionPressure overloadCardiomyocyte hypertrophyVascular mural cellsCardiomyocyte hypertrophy in vitroDecreased left ventricular hypertrophyStimulate cardiomyocyte hypertrophyCongenital heart defectsCell-specific knockoutLeft ventricular functionAdverse cardiac remodelingVentricular pressure overloadCardiomyocyte-specific deletionMural cellsHypertrophy in vitroPressure overload stressCardiac stromal cellsMyocardial tissue samplesEffects in vitroIn vitro studiesHypertrophy-related genesHeart defectsRegulate cardiac developmentVentricular function
2023
Characterizing the Spatiotemporal Transcriptomic Response of the Right Ventricle to Acute Pressure Overload
Kheyfets V, Kumar S, Heerdt P, Ichimura K, Brown R, Lucero M, Essafri I, Williams S, Stenmark K, Spiekerkoetter E. Characterizing the Spatiotemporal Transcriptomic Response of the Right Ventricle to Acute Pressure Overload. International Journal Of Molecular Sciences 2023, 24: 9746. PMID: 37298696, PMCID: PMC10253685, DOI: 10.3390/ijms24119746.Peer-Reviewed Original ResearchConceptsPressure overloadChronic RV pressure overloadExperimental pulmonary hypertension modelsRV pressure overloadTime pointsPulmonary hypertension modelRV outflow tractTranscriptomic signaturesAcute pressure overloadRight ventricular tissueDifferent time pointsPulmonary embolismHypertension modelSevere PEAcute increaseInitial insultOutflow tractRight ventricleRV apexVentricular tissueControl tissuesRatsSeverityWeeksTissue2.5D Flow MRI: 2D phase-contrast of the tricuspid valvular flow with automated valve-tracking
Lamy J, Xiang J, Seemann F, Gonzales R, Huber S, Steele J, Heiberg E, Peters D. 2.5D Flow MRI: 2D phase-contrast of the tricuspid valvular flow with automated valve-tracking. Proceedings Of The International Society For Magnetic Resonance In Medicine ... Scientific Meeting And Exhibition. 2023 DOI: 10.58530/2023/0930.Peer-Reviewed Original ResearchAssociated with diastolic dysfunctionTricuspid regurgitation velocityRV stroke volumePhase contrastDiastolic dysfunctionTricuspid regurgitationPulmonary hypertensionRegurgitation velocityPressure overloadRight heartHealthy subjectsTricuspidPhase contrast methodStroke volumeFlow MRIRegurgitationValvular flowPatientsPhase-dependent mannerFlow volumeEchocardiography
2022
Humanized Dsp ACM Mouse Model Displays Stress-Induced Cardiac Electrical and Structural Phenotypes
Stevens TL, Manring HR, Wallace MJ, Argall A, Dew T, Papaioannou P, Antwi-Boasiako S, Xu X, Campbell SG, Akar FG, Borzok MA, Hund TJ, Mohler PJ, Koenig SN, El Refaey M. Humanized Dsp ACM Mouse Model Displays Stress-Induced Cardiac Electrical and Structural Phenotypes. Cells 2022, 11: 3049. PMID: 36231013, PMCID: PMC9562631, DOI: 10.3390/cells11193049.Peer-Reviewed Original ResearchConceptsArrhythmogenic cardiomyopathyMouse modelStructural phenotypesFibro-fatty infiltrationFirst mouse modelHeart failureChamber dilationVentricular arrhythmiasPressure overloadArrhythmic eventsCardiac performanceCardiac stressSudden deathCardiovascular stressInherited disorderG variantConnexin 43MiceDesmosomal genesReduced expressionExternal stressorsACM familyDisease developmentMurine equivalentIncomplete penetrance
2021
MAP Kinase Phosphatase-5 Deficiency Protects Against Pressure Overload-Induced Cardiac Fibrosis
Zhong C, Min K, Zhao Z, Zhang C, Gao E, Huang Y, Zhang X, Baldini M, Roy R, Yang X, Koch WJ, Bennett AM, Yu J. MAP Kinase Phosphatase-5 Deficiency Protects Against Pressure Overload-Induced Cardiac Fibrosis. Frontiers In Immunology 2021, 12: 790511. PMID: 34992607, PMCID: PMC8724134, DOI: 10.3389/fimmu.2021.790511.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlood PressureCardiomegalyCells, CulturedDisease Models, AnimalDual-Specificity PhosphatasesEchocardiographyFibrosisHeartHeart FailureHumansInterleukin-4MacrophagesMaleMAP Kinase Signaling SystemMatrix Metalloproteinase 9MiceMice, KnockoutMyocardiumPhosphorylationPrimary Cell CultureVentricular RemodelingConceptsMitogen-activated protein kinase phosphatase 5Transverse aortic constrictionCardiac fibrosisMMP-9 expressionPressure overloadCardiac hypertrophyPressure overload-induced cardiac fibrosisOverload-induced cardiac fibrosisTAC-induced cardiac hypertrophyExcessive extracellular matrix depositionPro-fibrotic macrophagesCardiac pressure overloadP38 MAPKMatrix metalloproteinase-9Regulation of MMPsProtein kinase phosphatase 5JNK/ERKIL-4 stimulationExtracellular matrix depositionCardiac injuryAortic constrictionMyocardial fibrosisHeart diseaseFibrotic remodelingMetalloproteinase-9
2020
Dietary carbohydrates restriction inhibits the development of cardiac hypertrophy and heart failure
Nakamura M, Odanovic N, Nakada Y, Dohi S, Zhai P, Ivessa A, Yang Z, Abdellatif M, Sadoshima J. Dietary carbohydrates restriction inhibits the development of cardiac hypertrophy and heart failure. Cardiovascular Research 2020, 117: 2365-2376. PMID: 33070172, PMCID: PMC8861266, DOI: 10.1093/cvr/cvaa298.Peer-Reviewed Original ResearchMeSH Keywords3-Hydroxybutyric AcidAnimal FeedAnimalsCells, CulturedDiet, High-Protein Low-CarbohydrateDiet, KetogenicDietary CarbohydratesDisease Models, AnimalGlycogen Synthase Kinase 3 betaHeart FailureHemodynamicsHypertrophy, Left VentricularMaleMiceMice, Inbred C57BLMice, KnockoutMyocytes, CardiacNutritive ValueRatsRats, WistarSignal TransductionTOR Serine-Threonine KinasesVentricular Function, LeftVentricular RemodelingConceptsPressure overloadHeart failureDevelopment of cardiac hypertrophyLow-carbohydrateCardiac-specific knockout miceHigh carbohydrate control dietPhenylephrine-induced hypertrophyHypertensive cardiac remodelingDevelopment of pathological hypertrophyTransverse aortic constrictionWild-type miceAnti-hypertrophic mechanismsHearts of micePathological cardiac growthGSK-3bDietary carbohydrate restrictionSystolic dysfunctionAortic constrictionCardiac hypertrophyCardiac remodelingLC dietKnockout micePathological hypertrophyCarbohydrate restrictionCardiac pathologySLIT3 deficiency attenuates pressure overload-induced cardiac fibrosis and remodeling
Gong L, Wang S, Shen L, Liu C, Shenouda M, Li B, Liu X, Shaw J, Wineman A, Yang Y, Xiong D, Eichmann A, Evans SM, Weiss SJ, Si MS. SLIT3 deficiency attenuates pressure overload-induced cardiac fibrosis and remodeling. JCI Insight 2020, 5 PMID: 32644051, PMCID: PMC7406261, DOI: 10.1172/jci.insight.136852.Peer-Reviewed Original ResearchConceptsVentricular pressure overloadRight ventricular pressure overloadPressure overloadMyocardial fibrosisVentricular functionPressure overload-induced cardiac fibrosisLong-term ventricular functionOverload-induced cardiac fibrosisSlit guidance ligand 3Fibroblast activityPulmonary artery bandingPoor clinical outcomeTransverse aortic constrictionCongenital heart diseaseCollagen productionGlobal knockout micePotential therapeutic targetFibrillar collagen synthesisPulmonary hypertensionVentricular dysfunctionHemodynamic abnormalitiesOverall survivalAdverse remodelingClinical outcomesAfterload elevation
2019
Cardiomyocyte d-dopachrome tautomerase protects against heart failure
Ma Y, Su KN, Pfau D, Rao VS, Wu X, Hu X, Leng L, Du X, Piecychna M, Bedi K, Campbell SG, Eichmann A, Testani JM, Margulies KB, Bucala R, Young LH. Cardiomyocyte d-dopachrome tautomerase protects against heart failure. JCI Insight 2019, 4: e128900. PMID: 31484822, PMCID: PMC6777911, DOI: 10.1172/jci.insight.128900.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCalciumCardiomegalyCytokinesDisease Models, AnimalEchocardiographyGene DeletionGene ExpressionGenetic Predisposition to DiseaseHeart FailureHumansIntramolecular OxidoreductasesMaleMAP Kinase Kinase KinasesMiceMice, Inbred C57BLMice, KnockoutMyocytes, CardiacRecombinant ProteinsSignal TransductionTranscriptomeVascular Endothelial Growth Factor AConceptsTransverse aortic constrictionHeart failureRecombinant DDTConnective tissue growth factor expressionTissue growth factor expressionMore interstitial fibrosisAdvanced heart failureCardiac pressure overloadExperimental heart failureCardiac contractile dysfunctionLittermate control miceSmad-2 activationGrowth factor expressionSarcoplasmic reticulum calcium ATPaseMacrophage migration inhibitory factor (MIF) familyReticulum calcium ATPasePulmonary edemaCardiac dilatationContractile dysfunctionControl miceInterstitial fibrosisPressure overloadAntifibrotic actionAortic constrictionLow VEGFHigh-throughput single-molecule RNA imaging analysis reveals heterogeneous responses of cardiomyocytes to hemodynamic overload
Satoh M, Nomura S, Harada M, Yamaguchi T, Ko T, Sumida T, Toko H, Naito AT, Takeda N, Tobita T, Fujita T, Ito M, Fujita K, Ishizuka M, Kariya T, Akazawa H, Kobayashi Y, Morita H, Takimoto E, Aburatani H, Komuro I. High-throughput single-molecule RNA imaging analysis reveals heterogeneous responses of cardiomyocytes to hemodynamic overload. Journal Of Molecular And Cellular Cardiology 2019, 128: 77-89. PMID: 30611794, DOI: 10.1016/j.yjmcc.2018.12.018.Peer-Reviewed Original ResearchConceptsTransverse aortic constrictionHemodynamic overloadCardiomyocyte sizeExpression levelsGene expressionHeart failure stageSingle-cell RNA sequencingSingle-molecule RNAMyosin heavy chain βSingle-cell quantitative PCRFetal gene expressionFetal gene programSingle-cell analysis methodsSingle-molecule fluorescenceHeart failureSingle-cell levelPressure overloadAortic constrictionHypertrophy stageCardiac hypertrophyIsolated cardiomyocytesMyh7 expressionTemporal regulationRNA sequencingFetal genesGender-Related Differences in Transcatheter Aortic Valve Implantation
Stair B, Forrest J. Gender-Related Differences in Transcatheter Aortic Valve Implantation. 2019, 189-200. DOI: 10.1007/978-3-030-05912-5_16.Peer-Reviewed Original ResearchSurgical aortic valve replacementTranscatheter aortic valve implantationAortic valve implantationValve implantationSevere symptomatic aortic stenosisSymptomatic aortic stenosisAortic valve replacementLow surgical riskChronic pressure overloadStandard of careCardiovascular disease statesGender-related differencesTAVR studiesValve replacementAortic stenosisSurgical riskAdverse outcomesPressure overloadRisk factorsTreatment outcomesFemale genderFemale heartsPatientsDisease statesImpact of gender
2018
Cardiomyocyte gene programs encoding morphological and functional signatures in cardiac hypertrophy and failure
Nomura S, Satoh M, Fujita T, Higo T, Sumida T, Ko T, Yamaguchi T, Tobita T, Naito AT, Ito M, Fujita K, Harada M, Toko H, Kobayashi Y, Ito K, Takimoto E, Akazawa H, Morita H, Aburatani H, Komuro I. Cardiomyocyte gene programs encoding morphological and functional signatures in cardiac hypertrophy and failure. Nature Communications 2018, 9: 4435. PMID: 30375404, PMCID: PMC6207673, DOI: 10.1038/s41467-018-06639-7.Peer-Reviewed Original ResearchConceptsCardiac hypertrophyCardiomyocyte remodelingGene programHeart failurePressure overloadMorphological hypertrophyHeart functionHypertrophyP53 deletionEarly hypertrophyFunctional signaturesFunctional phenotypeLate hypertrophyP53 signalingTranscriptional signatureProgram activationMitochondrial inhibitionUnderlying mechanismCardiomyocyte identityCardiomyocytesMitochondrial activationRemodelingFailureTranscriptional programsActivation
2016
Endothelial Nogo-B regulates sphingolipid biosynthesis to promote the transition from hypertrophy to heart failure during chronic pressure overload
Zhang Y, Huang Y, Cantalupo A, Azevedo P, Siragusa M, Giordano F, Di Lorenzo A. Endothelial Nogo-B regulates sphingolipid biosynthesis to promote the transition from hypertrophy to heart failure during chronic pressure overload. International Journal Of Cardiology Cardiovascular Risk And Prevention 2016, 10: e2. DOI: 10.1016/j.jash.2016.03.006.Peer-Reviewed Original ResearchmiR-182 Modulates Myocardial Hypertrophic Response Induced by Angiogenesis in Heart
Li N, Hwangbo C, Jaba IM, Zhang J, Papangeli I, Han J, Mikush N, Larrivée B, Eichmann A, Chun HJ, Young LH, Tirziu D. miR-182 Modulates Myocardial Hypertrophic Response Induced by Angiogenesis in Heart. Scientific Reports 2016, 6: 21228. PMID: 26888314, PMCID: PMC4758045, DOI: 10.1038/srep21228.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCardiomegalyEndotheliumMechanistic Target of Rapamycin Complex 1Membrane ProteinsMiceMice, KnockoutMicroRNAsMultiprotein ComplexesMyocytes, CardiacNeovascularization, PathologicNitric OxideNitric Oxide Synthase Type IIIProteinsProto-Oncogene Proteins c-aktRGS ProteinsTOR Serine-Threonine KinasesUp-RegulationConceptsHypertrophic responseMiR-182Myocardial hypertrophyEndothelial-cardiomyocyte crosstalkLV pressure overloadEndothelium-derived NOPlacental growth factorMyocardial hypertrophic responseDevelopment of hypertrophyDegradation of regulatorsMiR-182 targetsHemodynamic demandsPressure overloadPlGF expressionBlood supplyParacrine actionCardiomyocyte hypertrophyMyocardial angiogenesisCardiac angiogenesisTreatment inhibitsHypertrophyAKT/mTORC1 pathwaysNovel targetAkt/Growth factor
2015
Natriuretic Peptides for Diagnosis, Prognosis, and Management of Heart Failure
Gandhi P, Januzzi Jr. J. Natriuretic Peptides for Diagnosis, Prognosis, and Management of Heart Failure. Biomarkers In Disease: Methods, Discoveries And Applications 2015, 731-756. DOI: 10.1007/978-94-007-7696-8_12.ChaptersB-type natriuretic peptideHeart failureNatriuretic peptideEjection fractionAmino-terminal pro-B-type natriuretic peptidePro-B-type natriuretic peptideHeart failure screeningReduced ejection fractionNatriuretic peptide releaseUse of biomarkersComplicated patientsRoutine carePressure overloadClinical assessmentMyocyte stretchCardiovascular homeostasisFluid balanceCardiac conditionsComplex syndromePatientsPersonalized carePeptide releaseMultiple studiesMillions of peopleCare
2014
Natriuretic Peptides for Diagnosis, Prognosis, and Management of Heart Failure
Gandhi P, Januzzi Jr. J. Natriuretic Peptides for Diagnosis, Prognosis, and Management of Heart Failure. 2014, 1-21. DOI: 10.1007/978-94-007-7740-8_12-1.ChaptersB-type natriuretic peptideHeart failureNatriuretic peptideEjection fractionAmino-terminal pro-B-type natriuretic peptidePro-B-type natriuretic peptideHeart failure screeningReduced ejection fractionNatriuretic peptide releaseUse of biomarkersComplicated patientsRoutine carePressure overloadClinical assessmentMyocyte stretchCardiovascular homeostasisFluid balanceCardiac conditionsComplex syndromePatientsPersonalized carePeptide releaseMultiple studiesMillions of peopleCare
2011
The ATP-Binding Cassette Transporter ABCG2 Protects Against Pressure Overload–Induced Cardiac Hypertrophy and Heart Failure by Promoting Angiogenesis and Antioxidant Response
Higashikuni Y, Sainz J, Nakamura K, Takaoka M, Enomoto S, Iwata H, Tanaka K, Sahara M, Hirata Y, Nagai R, Sata M. The ATP-Binding Cassette Transporter ABCG2 Protects Against Pressure Overload–Induced Cardiac Hypertrophy and Heart Failure by Promoting Angiogenesis and Antioxidant Response. Arteriosclerosis Thrombosis And Vascular Biology 2011, 32: 654-661. PMID: 22116099, DOI: 10.1161/atvbaha.111.240341.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornAntioxidantsATP Binding Cassette Transporter, Subfamily G, Member 2ATP-Binding Cassette TransportersCells, CulturedDisease Models, AnimalEndothelial CellsGenotypeGlutathioneHeart FailureHindlimbHumansHypertrophy, Left VentricularIschemiaMaleMiceMice, KnockoutMuscle, SkeletalMyocytes, CardiacNeoplasm ProteinsNeovascularization, PhysiologicOxidative StressPhenotypeRatsRats, WistarRNA InterferenceTime FactorsTransfectionVentricular FunctionVentricular RemodelingConceptsTransverse aortic constrictionWild-type micePressure overload-induced cardiac hypertrophyMicrovascular endothelial cellsOverload-induced cardiac hypertrophyCardiac hypertrophyHeart failureEndothelial cellsCassette transporter subfamily G member 2Exaggerated cardiac hypertrophyAntioxidant responseG member 2Tissue defense mechanismsSuperoxide dismutase mimeticCassette transporter ABCG2Cardiac dysfunctionImportant endogenous antioxidantPressure overloadVentricular remodelingAortic constrictionFunctional impairmentATP-Binding Cassette Transporter ABCG2Cardiomyocyte hypertrophyImpaired angiogenesisDismutase mimetic
1992
Hemodynamics of the Right Ventricle in Normal and Disease States
Lee F. Hemodynamics of the Right Ventricle in Normal and Disease States. Cardiology Clinics 1992, 10: 59-67. PMID: 1739960, DOI: 10.1016/s0733-8651(18)30255-8.Peer-Reviewed Original Research
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