grant
Attenuation of sepsis-induced microvascular permeability and inflammation with the GLP-1R agonist liraglutide.
Organization VANDERBILT UNIVERSITYLocation Nashville, UNITED STATESPosted 1 May 2025Deadline 31 May 2028
NIHUS FederalResearch GrantFY2026ASCVDAbdomenAdherens JunctionAdhering JunctionAdhesion MoleculeAdhesionsAdhesive JunctionAnchoring JunctionAnti-InflammatoriesAnti-Inflammatory AgentsAnti-inflammatoryAntiinflammatory EffectAtherosclerosisAtherosclerotic Cardiovascular DiseaseAttenuatedBlood CirculationBlood PlasmaBlood VesselsBlood leukocyteBlood monocyteBloodstreamBody TissuesBrain Vascular DisordersCCL2CCL2 geneCD54 AntigensCSAID-Binding Protein 1CSAID-Binding Protein 2CSBP2Cell Adhesion Molecule GeneCell Adhesion MoleculesCell BodyCell Communication and SignalingCell FunctionCell PhysiologyCell ProcessCell SignalingCell secretionCellsCellular FunctionCellular PhysiologyCellular ProcessCellular SecretionCerebrovascular DiseaseCerebrovascular DisordersCessation of lifeChemokine, CC Motif, Ligand 2Critical IllnessCritically IllCytokine-Suppressive Antiinflammatory Drug-Binding Protein 1Cytokine-Suppressive Antiinflammatory Drug-Binding protein 2DataDeathDiabetes MellitusDown-RegulationDrug TargetingDrugsDysfunctionEndothelial CellsEndotheliumFunctional disorderFundingGLP-1 RAGLP-1 agonistGLP-1 analogGLP-1 receptorGLP-1 receptor agonistGLP-I receptorGlucagon like peptide 1 agonistGlucagon like peptide-1 receptor agonistsGlucagon-like peptide-1 analogGoalsHumanHyperoxiaICAM-1Immune responseIn VitroInfectionInflammationInflammation MediatorsInflammatoryInjuryInjury to KidneyInjury to LiverIntercellular Adhesion MoleculesIntercellular adhesion molecule 1InterruptionIntracellular Communication and SignalingIntracranial Vascular DiseasesIntracranial Vascular DisordersLeukocyte TraffickingLeukocytesLeukocytes Reticuloendothelial SystemLifeLipopolysaccharidesLungLung Respiratory SystemLung damageMAP kinaseMAPK InhibitorsMAPK14MAPK14 Mitogen-Activated Protein KinaseMAPK14 geneMCAFMCP-1MCP1Marrow leukocyteMarrow monocyteMeasuresMediatingMedicationMiceMice MammalsMicrovascular PermeabilityMitogen-Activated Protein Kinase 14Mitogen-Activated Protein Kinase InhibitorMitogen-Activated Protein KinasesModelingModern ManMonocyte Chemoattractant Protein-1Monocyte Chemotactic Protein-1Monocyte Chemotactic and Activating FactorMonocyte Chemotactic and Activating ProteinMonocyte Chemotactive and Activating FactorMonocyte Secretory Protein JEMorbidityMurineMusMxi2Non obeseNonobeseObesityOccluding JunctionsOrganPathway interactionsPatientsPeripheralPermeabilityPharmaceutical PreparationsPhysiopathologyPlasmaPlasma SerumPrincipal InvestigatorProductionProteinsPulmonary EdemaRegulationReticuloendothelial System, Serum, PlasmaSAPK2ASCYA2SepsisSeveritiesSignal TransductionSignal Transduction SystemsSignalingSiteSmall Inducible Cytokine A2Stress-Activated Protein Kinase 2ASubcellular ProcessTestingTherapeuticTight JunctionsTissuesUpregulationVascular Endothelial CellVascular EndotheliumVascular PermeabilitiesWhite Blood CellsWhite CellWild Type MouseZonula Occludensadiposityanti-inflammatory effectantisepsis treatmentatheromatosisatherosclerotic diseaseatherosclerotic vascular diseaseattenuateattenuatesattenuationbiological signal transductionbrain vascular diseasebrain vascular dysfunctioncell adhesion proteincell typecerebral vascular diseasecerebral vascular dysfunctioncerebrovascular dysfunctionclinical efficacyclinical relevanceclinically relevantcorpulencecytokinediabetesdrug/agentexperimentexperimental researchexperimental studyexperimentsglucagon-like peptide-1 receptorhepatic damagehepatic injuryhost responsehyperoxygenationimmune system responseimmunoresponseimprovedin vitro Modelinflammatory mediatorinhibitorinjuriesinjury to organsintracranial vascular dysfunctionkidney injuryliraglutideliver damageliver injurylung edemalung injurylung microvascular endothelial cellslung vascular endothelial cellsmigrationmonocytemortalitymouse modelmurine modelnovelorgan injuryp38p38 MAP Kinasep38 MAPK Genep38 Mitogen Activated Protein Kinasep38 Protein Kinasep38 SAPKp38-Alphap38Alphapathophysiologypathwaypreservationprotective effectpulmonary damagepulmonary injurypulmonary microvascular endothelial cellspulmonary tissue damagepulmonary tissue injurypulmonary vascular endothelial cellsrecruitrenal injurysepsis caresepsis interventionssepsis managementsepsis therapeuticssepsis therapysepsis treatmentseptic therapyseptic treatmenttherapeutically effectivetreat sepsistreatment strategyvascularvascular inflammationwhite blood cellwhite blood corpusclewildtype mouse
Description preview
Project Abstract
Sepsis is a critical problem around the world causing 20% of all global deaths. The lack of effective
therapeutics leaves critically ill patients with systemic organ dysfunction often caused by damage to the
vascular endothelium. The damage induces micro-vessel dysfunction and increased permeability. Increased
permeability can be…
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