grant
NNMT Inhibition for treating heart failure
Organization UNIVERSITY OF CALIFORNIA LOS ANGELESLocation LOS ANGELES, UNITED STATESPosted 15 Aug 2025Deadline 31 May 2029
NIHUS FederalResearch GrantFY20253-PyridinecarboxamideAbscissionAddressAdoptedAmericanAnimal ModelAnimal Models and Related StudiesAnimalsAutophagocytosisBackBiogenesisCardiacCardiac Muscle CellsCardiac MyocytesCardiac infarctionCardiocyteCatabolismCausalityCause of DeathCessation of lifeCharacteristicsClinicalCoenzymesConsumptionCoupledDNA mutationDataDeathDefectDevelopmentDiastolic heart failureDihydronicotinamide Adenine DinucleotideDiphosphopyridine NucleotideDorsumDysfunctionEFRACEjection FractionEnzyme CofactorsEnzyme GeneEnzyme InductionEnzymesEtiologyEventExcisionExtirpationFunctional disorderGeneticGenetic ChangeGenetic ModelsGenetic defectGenetic mutationHF with preserved ejection fractionHFpEFHeartHeart Muscle CellsHeart failureHeart myocyteHumanImpairmentIntermediary MetabolismInvestigationInvestigatorsMetabolic ProcessesMetabolismMiceMice MammalsModelingModern ManMolecularMurineMusMutationMyocardialMyocardial InfarctMyocardial InfarctionMyocardial depressionMyocardial dysfunctionNMN pyrophosphorylaseNadideNiacinamideNicotinamideNicotinamide MononucleotideNicotinamide N-MethyltransferaseNicotinamide adenine dinucleotideNicotinamide-Adenine DinucleotideNicotinamidumNicotinic acid amideNicotylamideOrigin of LifePathogenesisPathologyPathway interactionsPellagra-Preventing FactorPhysiologicPhysiologicalPhysiopathologyPreventative strategyPreventionPrevention strategyPreventive strategyPrognosisPublishingRecyclingRemovalResearch PersonnelResearchersRiskSamplingSecondary toShuntShunt DeviceSilent Mating Type Information Regulator 2-like ProteinsSir2-like ProteinsSirtuinsStressStructureSupplementationSurgical RemovalTestingTherapeuticTherapeutic EffectTransferaseTransferase GeneVentricle RemodelingVentricular Cardiac RemodelingVentricular Myocardial RemodelingVentricular RemodelingVitamin B 3Vitamin B3Vitamin PPWorkautophagycardiac dysfunctioncardiac failurecardiac functioncardiac infarctcardiomyocytecausationcoenzyme analogcoronary attackcoronary infarctcoronary infarctiondevelopmentaldisease causationenzyme activityextracellularfunction of the heartgenome mutationheart attackheart dysfunctionheart failure and reduced ejection fractionheart failure with preserved ejection fractionheart failure with preserved systolic functionheart failure with reduced ejection fractionheart functionheart infarctheart infarctionhemodynamicshuman modelimprovedin vivoinhibitorinsightmetabolism measurementmetabolomemetabolomicsmetabonomemetabonomicsmodel of animalmodel of humanmortalitymouse modelmurine modelmyocardial remodelingnew therapeutic approachnew therapeutic interventionnew therapeutic strategiesnew therapy approachesnew treatment approachnew treatment strategynicotinamide methylasenicotinamide methyltransferasenicotinamide phosphoribosyltransferasenicotinamide ribonucleosidenicotinamide ribosenicotinamide ribosidenicotinamide-S-adenosylmethionine methyltransferasenicotinamide-beta-ribosidenovelnovel therapeutic approachnovel therapeutic interventionnovel therapeutic strategiesnovel therapy approachpathophysiologypathwaypharmacologicpre-clinicalpreclinicalpreservationpreserved ejection fraction heart failurepressurepreventpreventingresectionshuntssmall moleculetreatment strategy
Description preview
Project Summary
Heart failure (HF), spanning from HF with preserved ejection fraction (HFpEF) to HF with reduced ejection
fraction (HFrEF), is a leading cause of death worldwide, and among Americans, accounts for 14% of deaths at
present. Various pathophysiologic stresses have been clinically and experimentally identified to contribute to
HF via…
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