grant
Cellular Senescence and the AKI to CKD transition
Organization WASHINGTON UNIVERSITYLocation SAINT LOUIS, UNITED STATESPosted 5 Sept 2025Deadline 4 Sept 2029
NIHUS FederalResearch GrantFY2025AbscissionAcuteAcute Kidney FailureAcute Kidney InsufficiencyAcute Renal FailureAcute Renal InsufficiencyAddressAllelesAllelomorphsAreaAutomobile DrivingBasal Transcription FactorBasal transcription factor genesBilateralCell AgingCell CycleCell Cycle ArrestCell Cycle ControlCell Cycle ProgressionCell Cycle RegulationCell Division CycleCell SenescenceCellular AgingCellular SenescenceCellular injuryChronic Kidney FailureChronic Renal DiseaseChronic Renal FailureClinical ResearchClinical StudyCyclin GeneCyclinsDevelopmentDown-RegulationE3 LigaseE3 Ubiquitin LigaseElderlyEpithelial Cell ProliferationEpithelial CellsEpitheliumEvaluationEventExcisionExtirpationFKHL16FOXM1FOXM1 geneFOXM1BFamilyFamily memberFibrosisForkhead Box M1Forkhead Box M1B Transcription FactorForkhead, Drosophila, Homolog-Like 16G2/M ArrestGeneral Transcription Factor GeneGeneral Transcription FactorsGenesGeneticGenome InstabilityGenome StabilityGenomic InstabilityGenomic StabilityGoalsHFH11HistologicHistologicallyHospital AdmissionHospitalizationHumanImpairmentIn VitroIncidenceInjuryInjury to KidneyIschemia-Reperfusion InjuryKidneyKidney Urinary SystemKnowledgeLabelLeadMediatingMiceMice MammalsModern ManMolecularMurineMusPathway interactionsPatientsPb elementPhenotypePopulationPopulation StudyProcessProliferatingProteinsProteomicsPublishingRNA SeqRNA sequencingRNAseqRemovalRenal functionReperfusion DamageReperfusion InjuryReplicative SenescenceReporterRepressionRiskRoleSamplingSurgical RemovalTRIDENT geneTRIDENT proteinTestingTherapeutic InterventionTranscription Factor Proto-OncogeneTranscription factor genesTranslatingTubularTubular formationUbiquitilationUbiquitin Protein LigaseUbiquitin-Protein Ligase ComplexesUbiquitin-Protein Ligase E3UbiquitinationUbiquitinoylationUpregulationWorkacute kidney injuryadvanced ageattenuation of senescencecell damagecell injurycellular damagecellular developmentchronic kidney diseasecyclin Fdamage to cellsdecrease senescencedelay senescencedevelopmentaldrivingepithelial repairgeriatricheavy metal Pbheavy metal leadin vivoinjuredinjuriesinjury to cellsintervention therapykidney functionkidney injurykidney ischemiamouse modelmurine modelnovelpathwayphenotypic biomarkerphenotypic markerpopulation-based studypopulation-level studypre-clinical studypreclinical studypreventpreventingprogression riskreduce senescencereducing cellular senescencerenalrenal injuryrenal ischemiarepairrepairedreplicative agingrepress senescenceresectionresponsesenescencesenescence and its associated secretory phenotypesenescence associated secretomesenescence associated secretory factorssenescence associated secretory pathwaysenescence associated secretory phenotypesenescence associated secretory programsenescence associated secretory proteinssenescence mitigationsenescentsenescent associated secretomesenescent associated secretory phenotypesenior citizensenolyticssenomorphicsenostaticsocial rolestudies of populationsstudy of the populationsuppress senescencetranscription factortranscriptome sequencingtranscriptomic sequencingubiquinationubiquitin conjugationubiquitin-protein ligase
Description preview
PROJECT SUMMARY/ABSTRACT
Acute kidney injury (AKI) has a rising incidence among hospitalized patients and the risk for progression to
chronic kidney disease (CKD) has been established in both pre-clinical and clinical studies; however, there is
still a knowledge gap on the molecular mechanisms driving the AKI to CKD transition. We previously…
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