grant
Mitochondrial pp60Src and cellular metabolism in pulmonary vascular disease associated with CHD
Organization FLORIDA INTERNATIONAL UNIVERSITYLocation MIAMI, UNITED STATESPosted 10 Aug 2020Deadline 31 Jul 2030
NIHUS FederalResearch GrantFY20250-11 years oldAddressAffectAnabolismApoptoticAttentionAttenuatedBinding ProteinsBioenergeticsBirthBlood VesselsBlood flowBreathing MechanicsC-jun Amino-Terminal KinaseC-jun Kinase-1C-jun N-Terminal Kinase 1Cardiac MalformationCardiac defectCardiopulmonaryCell Communication and SignalingCell IsolationCell SegregationCell SeparationCell Separation TechnologyCell SignalingCellular Metabolic ProcessChildChild YouthChildren (0-21)CirculationCollagenComplexCongenital Cardiac DefectsCongenital Heart DefectsDataDepositDepositionDevelopmentDockingEPH- and ELK-Related Tyrosine KinaseEPH-and ELK-Related KinaseElectron TransportEndothelial CellsEndotheliumEphrin Type-A Receptor 8Ephrin Type-A Receptor 8 PrecursorExhibitsFundingGoalsHeart MalformationIncidenceIntermediary MetabolismInterventionIntervention StrategiesIntracellular Communication and SignalingInvestigationJN KinaseJNKJNK Mitogen-Activated Protein KinasesJNK1JNK1 KinaseJNK1 proteinJNK1A2JNK21B1/2KinasesL-ProlineLigand Binding ProteinLigand Binding Protein GeneLinkLive BirthLungLung Respiratory SystemMAP Kinase 8MAP Kinase 8 GeneMAPK8MAPK8 Mitogen-Activated Protein KinaseMAPK8 geneMediatingMedicalMetabolicMetabolic ProcessesMetabolismMitochondriaMitogen-Activated Protein Kinase 8ModelingMorbidityMorbidity - disease rateN-terminalNH2-terminalOperative ProceduresOperative Surgical ProceduresOuter Mitochondrial MembranePPAR gammaPPAR-gPPAR-γPPARgammaPPARγPRKM8ParturitionPeptidesPeroxisome Proliferative Activated Receptor GammaPeroxisome Proliferator-Activated Receptor gammaPeroxisome Proliferator-Activated Receptor γPhenotypePhosphorylationPhosphorylation SitePhosphotransferase GenePhosphotransferasesPhosphotyrosinePlayPost-Translational Modification Protein/Amino Acid BiochemistryPost-Translational ModificationsPost-Translational Protein ModificationPost-Translational Protein ProcessingPosttranslational ModificationsPosttranslational Protein ProcessingPreventionProcessProlineProtein BindingProtein ModificationProtein PhosphorylationProtein Tyrosine KinaseProtein Tyrosine Kinase EEKProteinsRegulationRespiratory MechanicsRiskRoleSAP Kinase-1SAPK/JNKSAPK1 Mitogen-Activated Protein KinaseSAPK1/JNKShuntShunt DeviceSignal TransductionSignal Transduction SystemsSignalingSiteStress-Activated Protein Kinase JNK1Stress-Activated Protein Kinase gammaSurgicalSurgical InterventionsSurgical ProcedureTechniquesTestingTherapeuticTherapeutic InterventionThiazolidinedione ReceptorTransphosphorylasesTyrosine KinaseTyrosine-O-phosphateTyrosine-Protein Kinase Receptor EEKTyrosine-Specific Protein KinaseTyrosylprotein Kinaseabnormal heart developmentabrogation of mitochondrial dysfunctionalleviating mitochondrial dysfunctionameliorating mitochondrial dysfunctionangiogenesisattenuateattenuatesattenuation of mitochondrial dysfunctionbiological signal transductionbiosynthesisbound proteinc-jun N-Terminal Kinasecell metabolismcell sortingcellular metabaolismcongenital cardiac abnormalitycongenital cardiac anomaliescongenital cardiac diseasecongenital cardiac disordercongenital cardiac malformationcongenital heart abnormalitycongenital heart anomalycongenital heart diseasecongenital heart disordercongenital heart malformationdesigndesigningdevelopmentalelectron transferendothelial dysfunctionfatty acid oxidationheart defecthemodynamicshydroxyaryl protein kinaseimpaired pulmonary vascularizationimprovedin vivoinsightintervention therapyjun-NH2-Terminal Kinasekidslamb modellung vascular diseasemitigating mitochondrial impairmentmitochondrialmitochondrial dysfunctionmitochondrial rejuvenationmortalitynovelpreventpreventingpulmonarypulmonary arterial endothelial cellpulmonary artery endothelial cellpulmonary vascular diseasepulmonary vascular disorderpulmonary vascular dysfunctionpulmonary vasculopathyreducing mitochondrial dysfunctionrestorationshuntssocial rolestress-activated protein kinase 1suppress mitochondrial dysfunctionsurgerytyrosyl protein kinasevascularvascular abnormalityyoungster
Description preview
ABSTRACT
Children born with congenital heart defects that cause pulmonary over-circulation develop abnormal pulmonary
vascular reactivity. Although survival has improved, they are at significant risk for developing pulmonary vascular
disease and continue to suffer morbidity and late mortality. Even early pulmonary endothelial dysfunction, with…
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