grant

Protein Translation for Oxidative Stress Response in Heart Failure

Organization UNIVERSITY OF ARIZONALocation TUCSON, UNITED STATESPosted 5 Sept 2025Deadline 31 Aug 2028
NIHUS FederalResearch GrantFY20255' Untranslated Regions5'UTRAbscissionAnimal ModelAnimal Models and Related StudiesAntioxidantsBasal Transcription FactorBasal transcription factor genesBindingBinding ProteinsBioinformaticsBody TissuesCardiacCardiac Muscle CellsCardiac MyocytesCardiac infarctionCardiocyteCell BodyCellsComplexDataData SetDeath RateDevelopmentDrug Metabolic DetoxicationDrug Metabolic DetoxificationEC 2.1.1Eukaryotic Initiation FactorsEukaryotic Peptide Initiation FactorsEukaryotic Translation Initiation FactorsExcisionExtirpationGene ExpressionGene TranscriptionGeneral Transcription Factor GeneGeneral Transcription FactorsGenesGenetic TranscriptionHeart InjuriesHeart Muscle CellsHeart failureHeart myocyteHumanIRESImpairmentInflammationIntermediary MetabolismInternal Ribosome Entry SegmentInternal Ribosome Entry SiteIschemic HeartIschemic Heart DiseaseIschemic myocardiumKnock-outKnockoutKnowledgeLab FindingsLabelLaboratoriesLaboratory FindingLifeLigand Binding ProteinLigand Binding Protein GeneLinkLiteratureMediatingMessenger RNAMeta-AnalysisMetabolic Drug DetoxicationsMetabolic ProcessesMetabolismMetabolism of Toxic AgentsMethylationMethyltransferaseMiceMice MammalsMitochondriaModern ManMolecularMolecular InteractionMurineMusMyocardial InfarctMyocardial InfarctionMyocardial IschemiaMyocardiumNF-E2-related factor 2Nova antigenNova proteinNrf2 proteinOxidantsOxidative StressOxidizing AgentsPatientsPolymerasePopulationProtein BindingProtein InhibitionProteinsProteomicsPublishingRNA ExpressionRNA methylationReactionReadingRemovalRibosome Entry SiteRibosomesSiteStressSurgical RemovalSystemTechniquesTestingTissuesTrans-Acting FactorsTrans-ActivatorsTransactivatorsTranscriptTranscriptionTranscription Factor Proto-OncogeneTranscription factor genesTranslatingTranslation InitiationTranslationsValidationVentricularWorkbiological adaptation to stressbound proteincardiac failurecardiac infarctcardiac injurycardiac ischemiacardiac musclecardiomyocytecohortcoronary attackcoronary infarctcoronary infarctioncoronary ischemiacostdetoxificationdevelopmentalelectron acceptorglobal gene expressionglobal transcription profileheart attackheart infarctheart infarctionheart ischemiaheart musclehuman datahuman diseaseindependencyinhibit proteininhibit proteinsischemia injuryischemic cardiomyopathyischemic injurymRNAmRNA Leader Sequencesmethylasemitochondrialmodel of animalmortality ratemortality ratiomyocardial ischemia/hypoxiamyocardium ischemiananopore based sequencingnanopore long read seqnanopore long-read sequencingnanopore seqnanopore sequencingnanopore-based long-read sequencingnovelprotein inhibitionsreaction; crisisrecruitrepairrepairedresectionstatisticsstress responsestress; reactiontherapeutic targettissue repairtranscription factortranscriptometranscriptomicstranslationtransmethylasevalidations
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ABSTRACT
A large volume of literature indicates an association of oxidative stress with the causes or progression of heart

failure. Heart failure is difficult to treat and costly to manage, yet carries a high mortality rate. Among the most

common causes of heart failure is myocardial ischemia or infarction. Lack of endogenous oxidant removal or…

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Protein Translation for Oxidative Stress Response in Heart Failure — UNIVERSITY OF ARIZONA | UNITED STATES | Sept 2025 | Dev Procure