Search results for "Pressure overload"

showing 10 items of 13 documents

Cardiomyocyte proliferation prevents failure in pressure overload but not volume overload

2017

Induction of the cell cycle is emerging as an intervention to treat heart failure. Here, we tested the hypothesis that enhanced cardiomyocyte renewal in transgenic mice expressing cyclin D2 would be beneficial during hemodynamic overload. We induced pressure overload by transthoracic aortic constriction (TAC) or volume overload by aortocaval shunt in cyclin D2-expressing and WT mice. Although cyclin D2 expression dramatically improved survival following TAC, it did not confer a survival advantage to mice following aortocaval shunt. Cardiac function decreased following TAC in WT mice, but was preserved in cyclin D2-expressing mice. On the other hand, cardiac structure and function were compr…

0301 basic medicineCardiac function curvemedicine.medical_specialtyAortic DiseasesVolume overloadCardiomegalyMice TransgenicConstriction Pathologic030204 cardiovascular system & hematologyMice03 medical and health sciences0302 clinical medicineCyclin D2FibrosisInternal medicinemedicineAnimalsCyclin D2Myocytes CardiacCell ProliferationCyclinHeart FailurePressure overloadbusiness.industryGeneral MedicineCell cyclemedicine.disease030104 developmental biologyEndocrinologyHeart failurebusinessResearch ArticleJournal of Clinical Investigation
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Reduced right atrial contractile force in patients with left ventricular diastolic dysfunction: A study in human atrial fibers—contractile force and …

2017

Summary Background/Objective The aim of our study was to evaluate right heart contractile force in patients with diastolic dysfunction (DD) with preserved left heart ejection fraction undergoing cardiac surgery. We examined the contractile properties of skinned human fibers obtained from the right auricle in two groups (DD and controls). Methods Right atrial tissue from 64 patients, who were undergoing cardiac surgery, were collected before extracorporal circulation. Tissue was conserved and prepared as "skinned fibers". We exposed the dissected fibers to increasing calcium concentrations and recorded the force values. Results Patients with DD develop significantly less force at middle and …

AdultMalemedicine.medical_specialtylcsh:SurgeryDiastoleAtrial Function Right030204 cardiovascular system & hematologyLeft ventricular hypertrophy030218 nuclear medicine & medical imagingVentricular Dysfunction Left03 medical and health sciences0302 clinical medicineDiastoleInternal medicineMitral valvemedicineHumansMitral valve prolapseskinned fiberAgedPressure overloadEjection fractionbusiness.industrylcsh:RD1-811Middle Agedmedicine.diseaseCardiac surgerymedicine.anatomical_structureCase-Control StudiesAortic valve stenosisCardiologyFemaleSurgerycalcium sensitivitydiastolic dysfunctionbusinessMuscle ContractionAsian Journal of Surgery
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Endothelial Leptin Receptor Deletion Promotes Cardiac Autophagy and Angiogenesis Following Pressure Overload by Suppressing Akt/mTOR Signaling.

2019

Background: Cardiac remodeling is modulated by overnutrition or starvation. The adipokine leptin mediates energy balance between adipose tissue and brain. Leptin and its receptors are expressed in the heart. Methods and Results: To examine the importance of endothelial leptin signaling in cardiac hypertrophy, transverse aortic constriction was used in mice with inducible endothelium-specific deletion of leptin receptors (End.LepR-KO) or littermate controls (End.LepR-WT). End.LepR-KO was associated with improved left ventricular function (fractional shortening, 28.4% versus 18.8%; P =0.0114), reduced left ventricular dilation (end-systolic inner left ventricular diameter, 3.59 versus 4.08 m…

AngiogenesisAdipose tissueAdipokineCardiomegaly030204 cardiovascular system & hematologyVentricular Function Left03 medical and health sciences0302 clinical medicineAutophagyMedicineAnimalsHumansGenetic Predisposition to Disease030212 general & internal medicineProtein kinase BCells Cultured2. Zero hungerPressure overloadHeart FailureMice KnockoutLeptin receptorNeovascularization Pathologicbusiness.industryLeptinMyocardiumTOR Serine-Threonine KinasesAutophagyEndothelial CellsFibrosisCell biologyDisease Models AnimalPhenotypeReceptors LeptinFemaleCardiology and Cardiovascular MedicinebusinessProto-Oncogene Proteins c-aktGene DeletionSignal TransductionCirculation. Heart failure
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Down-regulation of OPA1 alters mouse mitochondrial morphology, PTP function, and cardiac adaptation to pressure overload

2012

AIMS: The optic atrophy 1 (OPA1) protein is an essential protein involved in the fusion of the mitochondrial inner membrane. Despite its high level of expression, the role of OPA1 in the heart is largely unknown. We investigated the role of this protein in Opa1(+/-) mice, having a 50% reduction in OPA1 protein expression in cardiac tissue. METHODS AND RESULTS: In mutant mice, cardiac function assessed by echocardiography was not significantly different from that of the Opa1(+/+). Electron and fluorescence microscopy revealed altered morphology of the Opa1(+/-) mice mitochondrial network; unexpectedly, mitochondria were larger with the presence of clusters of fused mitochondria and altered c…

Cardiac function curveendocrine systemPhysiologyAdaptation BiologicalDown-RegulationBiologyMitochondrionMitochondrial Membrane Transport ProteinsPermeabilityGTP PhosphohydrolasesMitochondrial ProteinsMice03 medical and health sciencesMitochondrial membrane transport protein0302 clinical medicinePhysiology (medical)Optic Atrophy Autosomal DominantPressuremedicineAnimalsMyocyteMyocytes CardiacInner mitochondrial membrane030304 developmental biologyMice KnockoutPressure overload0303 health sciencesMitochondrial Permeability Transition Poremedicine.diseaseeye diseasesMitochondriaCell biologyBiochemistryMitochondrial permeability transition poreMitochondrial Membranesbiology.proteinOptic Atrophy 1Cardiology and Cardiovascular Medicine030217 neurology & neurosurgeryCardiovascular Research
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Procollagen C-Proteinase Enhancer 1 (PCPE-1) is a marker of myocardial fibrosis and impaired cardiac function in a murine model of pressure overload

2021

Abstract(1)AimsProcollagen C-proteinase enhancer 1 (PCPE-1) is an extracellular matrix protein and a major regulator of fibrillar collagen biosynthesis. Previous work has shown that its abundance is often increased in the context of tissue repair and fibrosis. The present study was designed to evaluate its potential as a biomarker of myocardial interstitial fibrosis (MIF), a well-established pathogenic pathway leading to heart failure.(2)Methods and ResultsCardiac fibrosis was induced in rats using an optimized model of chronic pressure overload triggered by angiotensin II and Nω-nitro-L-arginine methyl ester (L-NAME). All treated animals suffered from heart hypertrophy and the increase in …

Cardiac function curvemedicine.medical_specialtyCardiac fibrosis[SDV]Life Sciences [q-bio]Diastoleheart failure030204 cardiovascular system & hematology03 medical and health sciences0302 clinical medicineFibrosisInternal medicinemedicine030304 developmental biologyPressure overload0303 health sciencesCardiac fibrosiscirculating biomarkerbusiness.industrycollagen biosynthesismedicine.diseaseProcollagen C-proteinase enhancer 1 (PCPE-1)Angiotensin IIEndocrinologyHeart failureMyocardial fibrosisPET-MR imagingbusiness
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Inhibition of class I histone deacetylase with an apicidin derivative prevents cardiac hypertrophy and failure

2008

AIMS: Recent studies have demonstrated the importance of chromatin remodelling via histone acetylation/deacetylation for the control of cardiac gene expression. Specific histone deacetylases (HDACs) can, in fact, play a positive or negative role in determining cardiac myocyte (CM) size. Here, we report on the effect on hypertrophy development of three inhibitors (HDACi) of class I HDACs. METHODS AND RESULTS: The compounds were first analysed in vitro by scoring hypertrophy, expression of foetal genes, and apoptosis of neonatal rat CMs stimulated with phenylephrine, an alpha1-adrenergic agonist. This initial screening indicated that a truncated derivative of apicidin with class I HDAC specif…

Cardiac function curvemedicine.medical_specialtyHypertrophy Heart failurePhysiologymedicine.drug_classBiologyPeptides CyclicHistone DeacetylasesCell LineMuscle hypertrophychemistry.chemical_compoundPhysiology (medical)Internal medicinemedicineAnimalsHumansMyocytes CardiacEnzyme InhibitorsRats WistarCells CulturedHeart FailurePressure overloadHistone deacetylase inhibitorHypertrophic cardiomyopathyHypertrophymedicine.diseaseRatsHistone Deacetylase InhibitorsDisease Models AnimalEndocrinologychemistryEchocardiographyHeart failureHypertrophy Left VentricularHistone deacetylaseCardiology and Cardiovascular MedicineApicidinCardiovascular Research
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Myocardial maladaptation to pressure overload in CB2 receptor-deficient mice

2019

Abstract Background Adaptation to aortic valve stenosis leads to myocardial hypertrophy, which has been associated with inflammation, fibrosis and activation of the endocannabinoid system. Since the endocannabinoid system and the CB2 receptor provide cardioprotection and modulate immune response in experimental ischemia, we investigated the role of CB2 in a mouse model of cardiac pressure overload. Methods Transverse aortic constriction was performed in CB2 receptor-deficient (Cnr2−/−) mice and their wild-type littermates (Cnr2+/+). After echocardiography and Millar left heart catheter hemodynamic evaluation hearts were processed for histological, cellular and molecular analyses. Results Th…

Male0301 basic medicinemedicine.medical_specialtyGenotypeFluorescent Antibody TechniqueBlood PressureCardiomegalyInflammation030204 cardiovascular system & hematologyProinflammatory cytokineReceptor Cannabinoid CB2Mice03 medical and health sciences0302 clinical medicineImmune systemFibrosisInternal medicineVentricular DysfunctionmedicineAnimalsMyocytes CardiacMolecular BiologyMice KnockoutPressure overloadCardioprotectionVentricular RemodelingChemistryMyocardiumHemodynamicsmedicine.diseaseImmunohistochemistryEndocannabinoid systemDisease Models AnimalOxidative Stress030104 developmental biologyEndocrinologyFemaleInflammation Mediatorsmedicine.symptomCardiology and Cardiovascular MedicineMyofibroblastBiomarkersEndocannabinoidsJournal of Molecular and Cellular Cardiology
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Downregulation and Nuclear Relocation of MLP During the Progression of Right Ventricular Hypertrophy Induced by Chronic Pressure Overload

2000

Abstract The cardiac LIM domain protein MLP plays a crucial role in the architecture and mechanical function of cardiac myocytes. Mice lacking the MLP gene develop cardiac hypertrophy, dilated cardiopathy and heart failure. We investigated whether downregulation of MLP is induced by pressure overload and contributes to the physiopathology of cardiac hypertrophy and failure. We studied this mechanism in rat right ventricles submitted to pulmonary arterial hypertension, because it is known that this ventricle is very vulnerable to the deleterious effects of pressure overload. During the progression of cardiac hypertrophy to failure over a 31 days period there was a dramatic decrease by 50% of…

MaleCytoplasmmedicine.medical_specialtyTime FactorsTranscription GeneticHeart VentriclesDown-RegulationMuscle ProteinsCardiomegalyCytosolMyofibrilsDownregulation and upregulationRight ventricular hypertrophyInternal medicinePressureAnimalsVentricular FunctionMedicineMyocyteRNA MessengerRats WistarLungMolecular BiologyCell NucleusHomeodomain ProteinsPressure overloadReverse Transcriptase Polymerase Chain Reactionbusiness.industryMyocardiumLIM Domain Proteinsmedicine.diseaseImmunohistochemistryPulmonary hypertensionRatsMicroscopy Electronmedicine.anatomical_structureVentricleHeart failureCardiologyCardiology and Cardiovascular MedicinebusinessMyofibrilJournal of Molecular and Cellular Cardiology
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MiR-133 Modulates the β1Adrenergic Receptor Transduction Cascade.

2014

Rationale : The sympathetic nervous system plays a fundamental role in the regulation of myocardial function. During chronic pressure overload, overactivation of the sympathetic nervous system induces the release of catecholamines, which activate β-adrenergic receptors in cardiomyocytes and lead to increased heart rate and cardiac contractility. However, chronic stimulation of β-adrenergic receptors leads to impaired cardiac function, and β-blockers are widely used as therapeutic agents for the treatment of cardiac disease. MicroRNA-133 (miR-133) is highly expressed in the myocardium and is involved in controlling cardiac function through regulation of messenger RNA translation/stability. …

MalePhysiologyMessengerheart failureApoptosiscardiomyocytesInbred C57BLSecond Messenger SystemsTransgenicRats Sprague-DawleyBeta-1 adrenergic receptorMiceGenes ReporterReceptorsCyclic AMPGuanine Nucleotide Exchange FactorsMyocytes CardiacAlpha-1D adrenergic receptor3' Untranslated RegionsCells CulturedCulturedbiologyChemistryadrenergic beta-1 receptor antagonists; cardiac; cyclic AMP; heart failure; microRNAs; myocytes; 3' Untranslated Regions; Adenylyl Cyclases; Animals; Apoptosis; Cells Cultured; Cyclic AMP; Cyclic AMP-Dependent Protein Kinases; Disease Progression; Gene Expression Regulation; Genes Reporter; Guanine Nucleotide Exchange Factors; Male; Metoprolol; Mice; Mice Inbred C57BL; Mice Transgenic; MicroRNAs; Myocardium; Myocytes Cardiac; RNA Messenger; Rats; Rats Sprague-Dawley; Receptors Adrenergic beta-1; Recombinant Fusion Proteins; Second Messenger Systems; Physiology; Cardiology and Cardiovascular Medicine; Medicine (all)Medicine (all)Cell biologyAdrenergicadrenergic beta-1 receptor antagonistsDisease ProgressionCARDIAC HYPERTROPHYSignal transductionCardiology and Cardiovascular MedicineAdenylyl CyclasesMetoprololmedicine.medical_specialtyAdrenergic receptorcardiacCellsRecombinant Fusion ProteinsMice Transgenicbeta-1Alpha-1B adrenergic receptorInternal medicinecAMPmedicineAnimalsRNA MessengerReporterPressure overloadalpha and beta adrenoceptorsMyocytesMyocardiumBeta adrenergic receptor kinaseCyclic AMP-Dependent Protein KinasesAlpha-1A adrenergic receptorRatsMice Inbred C57BLMicroRNAsEndocrinologyGenesGene Expression Regulationbiology.proteinRNASprague-DawleyReceptors Adrenergic beta-1MicroRNAs; alpha and beta adrenoceptors; cardiomyocytes; CARDIAC HYPERTROPHY; cAMP
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Myocardial hypertrophy is associated with inflammation and activation of endocannabinoid system in patients with aortic valve stenosis.

2013

article i nfo Article history: Received 1 February 2013 Accepted 22 March 2013 Aims: Endocannabinoids and their receptors have been associated with cardiac adaptation to injury, inflam- mation and fibrosis. Experimental studies suggested a role for inflammatory reaction and active remodeling in myocardial hypertrophy, but they have not been shown in human hypertrophy. We investigated the asso- ciation of the endocannabinoid system with myocardial hypertrophy in patients with aortic stenosis. Main methods: Myocardial biopsies were collected from patients with aortic stenosis (AS) and atrial myxoma as controls during surgery. Histological and molecular analysis of endocannabinoids and their r…

Malemedicine.medical_specialtyInflammationCardiomegalyGeneral Biochemistry Genetics and Molecular BiologyMuscle hypertrophyFibrosisInternal medicinemedicineHumansGeneral Pharmacology Toxicology and PharmaceuticsAgedPressure overloadInflammationbiologybusiness.industryTenascin CGeneral MedicineAortic Valve Stenosismedicine.diseaseEndocannabinoid systemCTGFEndocrinologyAortic valve stenosisbiology.proteinlipids (amino acids peptides and proteins)Femalemedicine.symptombusinessEndocannabinoidsLife sciences
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