grant
Cardiomyocyte selective modulation of natriuretic peptide signaling in cardiomyopathy
Organization UNIVERSITY OF PITTSBURGH AT PITTSBURGHLocation PITTSBURGH, UNITED STATESPosted 9 Jul 2024Deadline 30 Jun 2028
NIHUS FederalResearch GrantFY2025ATP-protein phosphotransferaseAdenosine Cyclic Monophosphate-Dependent Protein KinasesAngiotensin ReceptorArrhythmiaAtrial Natriuretic FactorAtrial Natriuretic PeptidesAtriopeptinsAuriculinBNP Gene ProductBNP-32Basal Transcription FactorBasal transcription factor genesBasic Mechanisms of SUMOylationBiologyBrain Natriuretic Peptide-32Brain natriuretic peptideCD10 AntigensCREBCREB1CREB1 geneCalciumCardiacCardiac ArrhythmiaCardiac Failure CongestiveCardiac Muscle CellsCardiac MyocytesCardiocyteCardiomyopathiesCause of DeathCell Communication and SignalingCell SignalingChemicalsChronicClinical TrialsCongestive CardiomyopathyCongestive Heart FailureCyclic AMP-Dependent Protein KinasesCyclic GMPDataDefibrillatorsDevelopmentDilated CardiomyopathyDiseaseDisease ProgressionDisorderDrug TherapyElectric Shock Cardiac StimulatorsEnkephalinaseFutureGeneral Transcription Factor GeneGeneral Transcription FactorsGeneticGuanosine Cyclic MonophosphateHeartHeart ArrhythmiasHeart DecompensationHeart Muscle CellsHeart failureHeart myocyteHumanHyperpotassemiaHypotensionIndividualIntracellular Communication and SignalingKidney FailureKidney InsufficiencyKinase Family GeneLow Blood PressureMembrane MetalloendopeptidaseMethodsModelingModern ManMorbidityMorbidity - disease rateMyocardialMyocardial DiseasesMyocardial DisorderMyocardiopathiesNP proteinNatriuretic Factor-32Natriuretic Peptide HormonesNatriuretic PeptidesNeprilysinNesiritideNeutral EndopeptidasePIAS1 proteinPKAParticipantPathologicPathway interactionsPatientsPeptide Signal SequencesPharmacological TreatmentPharmacotherapyPhosphorylationPopulationPre-Clinical ModelPreclinical ModelsPredispositionProtein KinaseProtein Kinase AProtein PhosphorylationProteinsReducing AgentsReductantsRegulatory ProteinRenal FailureRenal InsufficiencyRiskRoleSERCA2aSUMOylationSecondary toSignal PathwaySignal PeptideSignal SequencesSignal TransductionSignal Transduction SystemsSignalingStimulators, Electrical, Cardiac, ShockStressSudden DeathSumoylation PathwaySusceptibilityTestingTherapeuticTranscription Factor Proto-OncogeneTranscription factor genesType-B Natriuretic PeptideVascular Hypotensive DisorderVentricular Arrhythmiaatrial natriuretic hormonebiological signal transductionbrain Natriuretic factorcAMP Response Element-Binding Protein 1cAMP-Dependent Protein KinasescGMPcardiac failurecardiac implantcardiomyocytechronic heart failuredevelopmentaldrug interventiondrug treatmentend stage diseasefamilial cardiomyopathygenetic cardiomyopathygenetic regulatory proteinglycogen synthase a kinasehereditary cardiomyopathyhydroxyalkyl protein kinasehyperkalemiaimprovedin vivoinherited cardiomyopathyinhibitormortalitymouse modelmurine modelmyocardium diseasemyocardium disordernon-geneticnongeneticpathwaypatient populationpharmaceutical interventionpharmacological interventionpharmacological therapypharmacology interventionpharmacology treatmentpharmacotherapeuticsphosphorylase b kinase kinasepre-clinicalpreclinicalpreventpreventingprotein inhibitor of activated STAT 1protein signal sequenceregulatory gene productresponseside effectsmall moleculesocial roletranscription factorvalsartan
Description preview
Project Summary:
In the last 30 years there has been a dramatic increase in our understanding of the genetic and non-genetic
mechanisms that contribute to the development of cardiomyopathy in humans. Despite this increased
mechanistic understanding, the risk of heart failure and sudden death remains high in this patient population.
While multiple…
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