grant
Mito-inflammation and sepsis-induced acute lung injury
Organization FLORIDA INTERNATIONAL UNIVERSITYLocation MIAMI, UNITED STATESPosted 21 Aug 2025Deadline 31 May 2029
NIHUS FederalResearch GrantFY2025ALI caused by sepsisARDSAcute Lung InjuryAcute Pulmonary InjuryAcute Respiratory DistressAcute Respiratory Distress SyndromeAdult ARDSAdult RDSAdult Respiratory Distress SyndromeAttenuatedAutophagocytosisAutoregulationBindingBreast CancerC-jun Amino-Terminal KinaseC-jun Kinase-1C-jun N-Terminal Kinase 1Cell Communication and SignalingCell SignalingCellular MatrixChemotactic CytokinesChimera ProteinChimeric ProteinsCritical CareCritical IllnessCritically IllCytoskeletal SystemCytoskeletonDa Nang LungDataDeath RateDephosphinDevelopmentDynaminDysfunctionEndothelial CellsEquilibriumFunctional disorderFusion ProteinGenerationsHomeostasisHomolog of Drosophila TOLLHomologous Chemotactic CytokinesImmune Cell ActivationImmunoglobulin Enhancer-Binding ProteinInfiltrationInflammasomeInflammationInflammatoryInflammatory ResponseInjuryIntercrinesIntracellular Communication and SignalingJN KinaseJNKJNK Mitogen-Activated Protein KinasesJNK1JNK1 KinaseJNK1 proteinJNK1A2JNK21B1/2KnowledgeLinkLungLung Respiratory SystemLung damageMAP Kinase 8MAP Kinase 8 GeneMAPK8MAPK8 Mitogen-Activated Protein KinaseMAPK8 geneMalignant Breast NeoplasmMalignant neoplasm of prostateMalignant prostatic tumorMediatingMitochondriaMitogen-Activated Protein Kinase 8MolecularMolecular InteractionNF-kBNF-kappa BNF-kappaBNFKBNitrogenNuclear Factor kappa BNuclear Transcription Factor NF-kBNucleotidesO elementO2 elementOxygenPRKM8PathologicPathway interactionsPatientsPhasePhysiological HomeostasisPhysiopathologyPlayPost-Translational Modification Protein/Amino Acid BiochemistryPost-Translational ModificationsPost-Translational Protein ModificationPost-Translational Protein ProcessingPosttranslational ModificationsPosttranslational Protein ProcessingPre-Clinical ModelPreclinical ModelsProcessProstate CAProstate CancerProstate malignancyProtein ModificationProteinsPublicationsPublishingReceptor ProteinRegulationRegulatory ProteinRoleSAP Kinase-1SAPK/JNKSAPK1 Mitogen-Activated Protein KinaseSAPK1/JNKSIS cytokinesScientific PublicationSepsisShock LungSignal TransductionSignal Transduction SystemsSignalingStiff lungStress-Activated Protein Kinase JNK1Stress-Activated Protein Kinase gammaTLR4TLR4 geneTestingTherapeuticToll HomologueTranscription Factor NF-kBTreatment EfficacyTubeWorkattenuateattenuatesautophagybalancebalance functionbiological signal transductionc-jun N-Terminal Kinasechemoattractant cytokinechemokinecustomized therapycustomized treatmentcytokinedenitrationdevelopmentaleffective therapyeffective treatmentgenetic regulatory proteinhuman diseaseimmune activationimprovedindividualized medicineindividualized patient treatmentindividualized therapeutic strategyindividualized therapyindividualized treatmentinjuriesinnovateinnovationinnovativeintervention efficacyintracellular skeletonjun-NH2-Terminal Kinasekappa B Enhancer Binding Proteinlung injurymalignant breast tumormitochondrialmortality ratemortality ratiomouse modelmurine modelnew drug treatmentsnew drugsnew pharmacological therapeuticnew therapeutic approachnew therapeutic interventionnew therapeutic strategiesnew therapeuticsnew therapynew therapy approachesnew treatment approachnew treatment strategynext generation therapeuticsnitrationnovelnovel drug treatmentsnovel drugsnovel pharmaco-therapeuticnovel pharmacological therapeuticnovel therapeutic approachnovel therapeutic interventionnovel therapeutic strategiesnovel therapeuticsnovel therapynovel therapy approachnuclear factor kappa betapathophysiologypathwaypatient specific therapiespatient specific treatmentpre-clinicalpreclinicalpreservationpulmonary damagepulmonary injurypulmonary tissue damagepulmonary tissue injuryreceptorrecruitregulatory gene productresponsesepsis associated ALIsepsis associated acute lung injurysepsis caused acute lung injurysepsis induced ALIsepsis induced acute lung injurysepsis mediated ALIsepsis mediated acute lung injurysepsis related acute lung injurysocial rolestress-activated protein kinase 1tailored medical treatmenttailored therapytailored treatmenttherapeutic agent developmenttherapeutic developmenttherapeutic efficacytherapeutic evaluationtherapeutic targettherapeutic testingtherapy efficacytoll-like receptor 4treatment strategyunique treatmentwet lung
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SUMMARY
Our prior work has shown that TLR4-mediated increases in mitochondrial (mt)-ROS play an essential role in the
inflammatory phase of acute lung injury (ALI) by stimulating NF-kB and nucleotide-binding domain-like receptor
protein 3 (NLRP3) inflammasome activity. However, the molecular mechanisms by which mt-ROS stimulates
inflammatory…
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