2024
Exploring a Novel Role of Glycerol Kinase 1 in Prostate Cancer PC-3 Cells
Park B, Kim S, Yu S, Kim K, Jeon H, Ahn S. Exploring a Novel Role of Glycerol Kinase 1 in Prostate Cancer PC-3 Cells. Biomolecules 2024, 14: 997. PMID: 39199385, PMCID: PMC11352368, DOI: 10.3390/biom14080997.Peer-Reviewed Original ResearchPC-3 cellsProstate cancer PC-3 cellsGK deficiencyCell deathProstate cancerAnti-cancer agentsKinase 1Apoptotic cell deathDNA microarray analysisHuman prostate cancer PC-3 cellsCancer cell deathModulating tumor microenvironmentProstate cancer cellsBiomarkers of cell deathX chromosomeReduced cell viabilityEpigenetic regulationExpression vectorInvestigated genesSynthesis of triglyceridesMicroarray analysisGenetic alterationsTumor microenvironmentNovel roleCancer cellsGeneration of transmitochondrial cybrids in cancer cells
Soler-Agesta R, Ripollés-Yuba C, Marco-Brualla J, Moreno-Loshuertos R, Sato A, Beltrán-Visiedo M, Galluzzi L, Anel A. Generation of transmitochondrial cybrids in cancer cells. Methods In Cell Biology 2024, 189: 23-40. PMID: 39393884, DOI: 10.1016/bs.mcb.2024.05.010.Peer-Reviewed Original ResearchTransmitochondrial cybridsCancer cellsApoptotic cell deathSource of ATPCancer cell functionsMitochondrial genomeCircular genomeNuclear genesMitochondrial DNATransfer RNAMitochondrial proteinsRibosomal RNAMitochondrial componentsIntact mitochondriaMitochondrial functionCybridsCell deathMetabolic intermediatesMitochondriaGenomeCell functionRNACellsTumor progressionAbundant source
2023
Harnessing small extracellular vesicles for pro-oxidant delivery: novel approach for drug-sensitive and resistant cancer therapy
Kang C, Ren X, Lee D, Ramesh R, Nimmo S, Yang-Hartwich Y, Kim D. Harnessing small extracellular vesicles for pro-oxidant delivery: novel approach for drug-sensitive and resistant cancer therapy. Journal Of Controlled Release 2023, 365: 286-300. PMID: 37992875, PMCID: PMC10872719, DOI: 10.1016/j.jconrel.2023.11.031.Peer-Reviewed Original ResearchSmall extracellular vesiclesMDR cancer cellsMultidrug resistanceCancer cellsDrug resistanceReactive oxygen speciesExtracellular vesiclesOvarian cancer cellsDrug-resistant cancersApoptotic cell deathCancer treatment strategiesTreatment strategiesTherapy highlightClinical problemMDR tumorsDrug responsivenessP-glycoproteinPotent anticancer activityCancer treatmentRedox balanceATP productionOxidative stressTumorsVivo studiesMitochondrial dysfunctionNegative feedback regulation of MAPK signaling is an important driver of chronic lymphocytic leukemia progression
Ecker V, Brandmeier L, Stumpf M, Giansanti P, Moreira A, Pfeuffer L, Fens M, Lu J, Kuster B, Engleitner T, Heidegger S, Rad R, Ringshausen I, Zenz T, Wendtner C, Müschen M, Jellusova J, Ruland J, Buchner M. Negative feedback regulation of MAPK signaling is an important driver of chronic lymphocytic leukemia progression. Cell Reports 2023, 42: 113017. PMID: 37792532, DOI: 10.1016/j.celrep.2023.113017.Peer-Reviewed Original ResearchConceptsMitogen-activated protein kinaseChronic lymphocytic leukemiaCLL cellsMitochondrial reactive oxygen speciesChronic lymphocytic leukemia progressionApoptotic cell deathPoor clinical prognosisCLL cell survivalSmall molecule inhibitorsNegative feedback regulationProtein kinaseReactive oxygen speciesMAPK signalingMAPK activityPromising treatment conceptClinical prognosisClinical challengeLymphocytic leukemiaCell survivalAcute activationCell deathDNA damageDUSP6Treatment conceptFeedback regulationEffector response to necroptotic cell death: an ensemble of immune and stromal cells
Hughes L, Altun O, Nevin J, Wang M, Kluger Y, Pelorosso F, Leighton J, Rothlin C, Ghosh S. Effector response to necroptotic cell death: an ensemble of immune and stromal cells. The Journal Of Immunology 2023, 210: 72.39-72.39. DOI: 10.4049/jimmunol.210.supp.72.39.Peer-Reviewed Original ResearchApoptotic cell deathCell deathGene expression programsEffector responsesNecroptotic cell deathSingle-cell levelMyofibroblast transitionExpression programsStromal cellsTissue renewalTranscriptomic changesCellular corpsesInflammatory bowel diseaseExcessive inflammatory responseInfluence of TGFChemo-genetic approachNon-resolving inflammationMolecular pathwaysResolution of inflammationEssential roleMajor stromal cellsBowel diseaseInflammatory responseInjury modelHelminth infectionsApoptotic cell death in disease—Current understanding of the NCCD 2023
Vitale I, Pietrocola F, Guilbaud E, Aaronson S, Abrams J, Adam D, Agostini M, Agostinis P, Alnemri E, Altucci L, Amelio I, Andrews D, Aqeilan R, Arama E, Baehrecke E, Balachandran S, Bano D, Barlev N, Bartek J, Bazan N, Becker C, Bernassola F, Bertrand M, Bianchi M, Blagosklonny M, Blander J, Blandino G, Blomgren K, Borner C, Bortner C, Bove P, Boya P, Brenner C, Broz P, Brunner T, Damgaard R, Calin G, Campanella M, Candi E, Carbone M, Carmona-Gutierrez D, Cecconi F, Chan F, Chen G, Chen Q, Chen Y, Cheng E, Chipuk J, Cidlowski J, Ciechanover A, Ciliberto G, Conrad M, Cubillos-Ruiz J, Czabotar P, D’Angiolella V, Daugaard M, Dawson T, Dawson V, De Maria R, De Strooper B, Debatin K, Deberardinis R, Degterev A, Del Sal G, Deshmukh M, Di Virgilio F, Diederich M, Dixon S, Dynlacht B, El-Deiry W, Elrod J, Engeland K, Fimia G, Galassi C, Ganini C, Garcia-Saez A, Garg A, Garrido C, Gavathiotis E, Gerlic M, Ghosh S, Green D, Greene L, Gronemeyer H, Häcker G, Hajnóczky G, Hardwick J, Haupt Y, He S, Heery D, Hengartner M, Hetz C, Hildeman D, Ichijo H, Inoue S, Jäättelä M, Janic A, Joseph B, Jost P, Kanneganti T, Karin M, Kashkar H, Kaufmann T, Kelly G, Kepp O, Kimchi A, Kitsis R, Klionsky D, Kluck R, Krysko D, Kulms D, Kumar S, Lavandero S, Lavrik I, Lemasters J, Liccardi G, Linkermann A, Lipton S, Lockshin R, López-Otín C, Luedde T, MacFarlane M, Madeo F, Malorni W, Manic G, Mantovani R, Marchi S, Marine J, Martin S, Martinou J, Mastroberardino P, Medema J, Mehlen P, Meier P, Melino G, Melino S, Miao E, Moll U, Muñoz-Pinedo C, Murphy D, Niklison-Chirou M, Novelli F, Núñez G, Oberst A, Ofengeim D, Opferman J, Oren M, Pagano M, Panaretakis T, Pasparakis M, Penninger J, Pentimalli F, Pereira D, Pervaiz S, Peter M, Pinton P, Porta G, Prehn J, Puthalakath H, Rabinovich G, Rajalingam K, Ravichandran K, Rehm M, Ricci J, Rizzuto R, Robinson N, Rodrigues C, Rotblat B, Rothlin C, Rubinsztein D, Rudel T, Rufini A, Ryan K, Sarosiek K, Sawa A, Sayan E, Schroder K, Scorrano L, Sesti F, Shao F, Shi Y, Sica G, Silke J, Simon H, Sistigu A, Stephanou A, Stockwell B, Strapazzon F, Strasser A, Sun L, Sun E, Sun Q, Szabadkai G, Tait S, Tang D, Tavernarakis N, Troy C, Turk B, Urbano N, Vandenabeele P, Vanden Berghe T, Vander Heiden M, Vanderluit J, Verkhratsky A, Villunger A, von Karstedt S, Voss A, Vousden K, Vucic D, Vuri D, Wagner E, Walczak H, Wallach D, Wang R, Wang Y, Weber A, Wood W, Yamazaki T, Yang H, Zakeri Z, Zawacka-Pankau J, Zhang L, Zhang H, Zhivotovsky B, Zhou W, Piacentini M, Kroemer G, Galluzzi L. Apoptotic cell death in disease—Current understanding of the NCCD 2023. Cell Death & Differentiation 2023, 30: 1097-1154. PMID: 37100955, PMCID: PMC10130819, DOI: 10.1038/s41418-023-01153-w.Peer-Reviewed Original ResearchConceptsRegulated cell deathCell deathAdult tissue homeostasisMultiple human disordersApoptotic cell deathOrganismal developmentOrganismal homeostasisMolecular machineryContext of diseaseApoptotic apparatusMammalian systemsCaspase familyTissue homeostasisGenetic strategiesHuman disordersNomenclature CommitteeApoptosisHomeostasisMachineryOncogenesisProteaseCell lossActivationFamilyDeathNLRX1 knockdown attenuates pro-apoptotic signaling and cell death in pulmonary hyperoxic acute injury
Kim H, Kim M, Kim E, Leem J, Baek S, Lee Y, Kim K, Kang M, Song T, Sohn M. NLRX1 knockdown attenuates pro-apoptotic signaling and cell death in pulmonary hyperoxic acute injury. Scientific Reports 2023, 13: 3441. PMID: 36859435, PMCID: PMC9975446, DOI: 10.1038/s41598-023-28206-x.Peer-Reviewed Original ResearchConceptsHyperoxic acute lung injuryAcute lung injuryLung injuryWT miceAcute respiratory failurePro-inflammatory cytokinesCell deathRespiratory failureAcute injuryInflammatory cellsReduced mortalityRole of NLRX1Murine modelNLRX1 expressionPro-apoptotic signalingCell cytotoxicityHyperoxiaInjuryMiceProtein leakageHyperoxic conditionsNLRX1Apoptotic cell deathERK 1/2Reactive oxygen species
2022
TOP1-DNA Trapping by Exatecan and Combination Therapy with ATR Inhibitor.
Jo U, Murai Y, Agama KK, Sun Y, Saha LK, Yang X, Arakawa Y, Gayle S, Jones K, Paralkar V, Sundaram RK, Van Doorn J, Vasquez JC, Bindra RS, Choi WS, Pommier Y. TOP1-DNA Trapping by Exatecan and Combination Therapy with ATR Inhibitor. Molecular Cancer Therapeutics 2022, 21: 1090-1102. PMID: 35439320, PMCID: PMC9256811, DOI: 10.1158/1535-7163.mct-21-1000.Peer-Reviewed Original ResearchConceptsATR inhibitorsTop1 inhibitorsHomologous recombination deficiencyNovel molecular interactionApoptotic cell deathCancer cellsTop1 cleavage complexesAtaxia telangiectasiaCleavage complexesCell deathDNA damageHigher DNA damageMolecular interactionsDNA baseKinase inhibitorsI inhibitorMolecular pharmacologyMouse xenograftsTOP1Recombination deficiencyTopoisomerase I inhibitorInhibitorsTumor growthRad3Predictive biomarkersIntegrative molecular and clinical profiling of acral melanoma links focal amplification of 22q11.21 to metastasis
Farshidfar F, Rhrissorrakrai K, Levovitz C, Peng C, Knight J, Bacchiocchi A, Su J, Yin M, Sznol M, Ariyan S, Clune J, Olino K, Parida L, Nikolaus J, Zhang M, Zhao S, Wang Y, Huang G, Wan M, Li X, Cao J, Yan Q, Chen X, Newman AM, Halaban R. Integrative molecular and clinical profiling of acral melanoma links focal amplification of 22q11.21 to metastasis. Nature Communications 2022, 13: 898. PMID: 35197475, PMCID: PMC8866401, DOI: 10.1038/s41467-022-28566-4.Peer-Reviewed Original ResearchConceptsAcral melanomaMelanoma subtypesClinical profilingCommon melanoma subtypeImmune checkpoint blockadeCheckpoint blockadeInferior survivalMelanoma cell linesKey molecular driversPoor prognosisTherapeutic targetAnchorage-independent growthImmunomodulatory genesNon-white individualsHotspot mutationsMolecular driversCandidate oncogeneMelanomaApoptotic cell deathLZTR1Focal amplificationTumor promoterCell linesMetastasisTumor suppressor
2020
Dual role of reactive oxygen species in autophagy and apoptosis induced by compound PN in prostate cancer cells
Choi H, Kim K, Park K, Kim S, Park S, Yu S, Kim Y, Kim D, Chung K, Ahn S. Dual role of reactive oxygen species in autophagy and apoptosis induced by compound PN in prostate cancer cells. Molecular & Cellular Toxicology 2020, 17: 41-50. DOI: 10.1007/s13273-020-00107-4.Peer-Reviewed Original ResearchMitochondrial reactive oxygen speciesReactive oxygen speciesCell deathMolecular mechanismsProstate cancer cellsPC-3 cellsCell survivalAnti-cancer activityROS productionApoptotic cell deathCancer cellsOxygen speciesROS-dependent mannerInduction of apoptosisProstate cancer PC-3 cellsHuman prostate cancer cellsAcceleration of apoptosisCancer PC-3 cellsInhibition of autophagyProduction of intracellularIntracellular ROS scavengerProstate cancer treatmentExpression of apoptosisAutophagy inductionWestern blot analysisSingle-day Postnatal Alcohol Exposure Induces Apoptotic Cell Death and Causes long-term Neuron Loss in Rodent Thalamic Nucleus Reuniens
Gursky ZH, Spillman EC, Klintsova AY. Single-day Postnatal Alcohol Exposure Induces Apoptotic Cell Death and Causes long-term Neuron Loss in Rodent Thalamic Nucleus Reuniens. Neuroscience 2020, 435: 124-134. PMID: 32251710, PMCID: PMC7236664, DOI: 10.1016/j.neuroscience.2020.03.046.Peer-Reviewed Original ResearchConceptsFetal alcohol spectrum disordersAlcohol exposureThalamic nucleus reuniensCell lossAlcohol administrationFemale Long-Evans rat pupsNucleus reuniensApoptotic cell deathNon-neuronal cell numbersThird trimester alcohol exposureLong-Evans rat pupsCell deathPostnatal alcohol exposureAlcohol-exposed animalsFunction of hippocampusDevelopmental alcohol exposurePostnatal day 7Evans rat pupsEarly life stressAlcohol spectrum disordersCell numberCell type-dependent mannerNeuron lossRat pupsRodent models
2019
Phase 1, first-in-human study of TRAIL receptor agonist fusion protein ABBV-621.
Ratain M, Doi T, De Jonge M, LoRusso P, Dunbar M, Chiney M, Motwani M, Glasgow J, Petrich A, Rasco D, Calvo E. Phase 1, first-in-human study of TRAIL receptor agonist fusion protein ABBV-621. Journal Of Clinical Oncology 2019, 37: 3013-3013. DOI: 10.1200/jco.2019.37.15_suppl.3013.Peer-Reviewed Original ResearchDose escalationDose-limiting toxicityBlood-based markersECOG 0Prior regimensStable diseaseAcceptable toxicityMedian durationRespiratory failureMedian agePartial responseColorectal cancerPancreatic cancerBlood bilirubinBayesian continual reassessment methodPD markersContinual reassessment methodHuman studiesDay 1Solid tumorsTumor typesPK studiesTumor modelAntitumor activityApoptotic cell deathSynergistic activity of BET inhibitor MK-8628 and PLK inhibitor Volasertib in preclinical models of medulloblastoma
Han Y, Lindner S, Bei Y, Garcia H, Timme N, Althoff K, Odersky A, Schramm A, Lissat A, Künkele A, Deubzer H, Eggert A, Schulte J, Henssen A. Synergistic activity of BET inhibitor MK-8628 and PLK inhibitor Volasertib in preclinical models of medulloblastoma. Cancer Letters 2019, 445: 24-33. PMID: 30611741, DOI: 10.1016/j.canlet.2018.12.012.Peer-Reviewed Original ResearchConceptsModel of medulloblastomaMYC-amplified medulloblastomaMK-8628Preclinical models of medulloblastomaAnti-tumor effectsPreclinical modelsTherapeutic efficacyCentral nervous system tumorsAggressive clinical courseHigh-risk medulloblastomaTherapy-related morbidityCurrent treatment regimensNervous system tumorsTargeted treatment approachesBET protein BRD4MYC protein stabilityIn vivo modelsMYC amplificationMedulloblastoma modelApoptotic cell deathCell cycle arrestClinical courseTreatment regimensSystem tumorsTarget of Plk1
2017
Synucleinopathies in neurodegenerative diseases: Accomplices, an inside job and selective vulnerability
Azizi S, Azizi S. Synucleinopathies in neurodegenerative diseases: Accomplices, an inside job and selective vulnerability. Neuroscience Letters 2017, 672: 150-152. PMID: 29217261, DOI: 10.1016/j.neulet.2017.12.003.Peer-Reviewed Original ResearchDeath begets a new beginning
Bosurgi L, Hughes LD, Rothlin CV, Ghosh S. Death begets a new beginning. Immunological Reviews 2017, 280: 8-25. PMID: 29027219, PMCID: PMC5658037, DOI: 10.1111/imr.12585.BooksConceptsCell deathBillions of cellsApoptotic cell deathEnvironmental cuesSpecific functionsHomeostatic conditionsTissue microenvironmentApoptotic cellsDead cellsTissue repairGrowth factorCellsPhagocytosisPerpetual featureSevere tissue injuryDeathInductionAppropriate responseMicroenvironmentPhagocytesCues
2016
Inhibition of Regulatory-Associated Protein of Mechanistic Target of Rapamycin Prevents Hyperoxia-Induced Lung Injury by Enhancing Autophagy and Reducing Apoptosis in Neonatal Mice
Sureshbabu A, Syed M, Das P, Janér C, Pryhuber G, Rahman A, Andersson S, Homer RJ, Bhandari V. Inhibition of Regulatory-Associated Protein of Mechanistic Target of Rapamycin Prevents Hyperoxia-Induced Lung Injury by Enhancing Autophagy and Reducing Apoptosis in Neonatal Mice. American Journal Of Respiratory Cell And Molecular Biology 2016, 55: 722-735. PMID: 27374190, PMCID: PMC5105179, DOI: 10.1165/rcmb.2015-0349oc.Peer-Reviewed Original ResearchMeSH KeywordsAcute Lung InjuryAdaptor Proteins, Signal TransducingAlveolar Epithelial CellsAnimalsAnimals, NewbornApoptosisAutophagyBronchopulmonary DysplasiaCell LineFemaleHumansHyperoxiaHypertension, PulmonaryHypertrophy, Right VentricularInfant, NewbornLungMiceMicrotubule-Associated ProteinsNaphthyridinesPhenotypeRegulatory-Associated Protein of mTORTime FactorsTumor Suppressor Protein p53ConceptsAcute lung injuryBronchopulmonary dysplasiaLung injuryWild-type miceMechanistic targetRegulatory-Associated ProteinLysosomal-associated membrane protein 1Apoptotic cell deathFetal type II alveolar epithelial cellsMouse lungRole of autophagyHyperoxia-Induced Lung InjuryLight chain 3Activation of autophagyType II alveolar epithelial cellsRespiratory distress syndromeMembrane protein 1Developmental lung diseaseUseful therapeutic targetNeonatal mouse lungAlveolar epithelial cellsPharmacological inhibitorsTreatment of hyperoxiaCell deathAutophagic fluxExpression of FADD and cFLIPL balances mitochondrial integrity and redox signaling to substantiate apoptotic cell death
Ranjan K, Pathak C. Expression of FADD and cFLIPL balances mitochondrial integrity and redox signaling to substantiate apoptotic cell death. Molecular And Cellular Biochemistry 2016, 422: 135-150. PMID: 27619661, DOI: 10.1007/s11010-016-2813-z.Peer-Reviewed Original ResearchConceptsExpression of FADDMitochondrial integrityCell deathDeath receptorsMutant of FADDInduced expressionNon-apoptotic functionsDeath receptor signalingFate of cellsMitochondrial-associated apoptosisApoptotic cell deathCancer cellsCellular signalingEctopic expressionJNK1 activationFADDCellular respirationHA14-1Independent pathwaysReceptor signalingCFLIPCFLIPLBcl-2ApoptosisIntracellular ROSFADD regulates NF-κB activation and promotes ubiquitination of cFLIPL to induce apoptosis
Ranjan K, Pathak C. FADD regulates NF-κB activation and promotes ubiquitination of cFLIPL to induce apoptosis. Scientific Reports 2016, 6: 22787. PMID: 26972597, PMCID: PMC4789601, DOI: 10.1038/srep22787.Peer-Reviewed Original ResearchMeSH KeywordsA549 CellsAnimalsApoptosisBaculoviral IAP Repeat-Containing 3 ProteinBlotting, WesternCASP8 and FADD-Like Apoptosis Regulating ProteinCaspase 8Cell LineCell SurvivalFas-Associated Death Domain ProteinHCT116 CellsHEK293 CellsHeLa CellsHT29 CellsHumansInhibitor of Apoptosis ProteinsMCF-7 CellsMiceNF-kappa BNIH 3T3 CellsProtein BindingRepressor ProteinsRNA InterferenceTumor Necrosis Factor-alphaUbiquitin-Protein LigasesUbiquitinationConceptsCell deathProcaspase-8Molecular mechanismsCellular FLICE-like inhibitory proteinFLICE-like inhibitory proteinExpression of cFLIPLCell death signalingApoptosis protein 2Apoptotic cell death signalingHEK 293T cellsNovel molecular mechanismApoptotic cell deathNF-κB activationFasL stimulationCellular inhibitorE3 ubiquitinTNF-α stimulationDeath domainDeath inducingDeath signalingEctopic expressionFADDCaspase-8NF-κBCell survivalAutophagy ameliorates cognitive impairment through activation of PVT1 and apoptosis in diabetes mice
Li Z, Hao S, Yin H, Gao J, Yang Z. Autophagy ameliorates cognitive impairment through activation of PVT1 and apoptosis in diabetes mice. Behavioural Brain Research 2016, 305: 265-277. PMID: 26971628, DOI: 10.1016/j.bbr.2016.03.023.Peer-Reviewed Original ResearchMeSH KeywordsAdenineAnimalsAntibiotics, AntineoplasticApoptosisAutophagyBeclin-1Body WeightCognition DisordersDiabetes Mellitus, ExperimentalDisease Models, AnimalEatingExploratory BehaviorHippocampusHypoglycemic AgentsLong-Term PotentiationMaleMaze LearningMiceMice, Inbred C57BLMicrotubule-Associated ProteinsPerforant PathwayRNA, Long NoncodingStreptozocinConceptsDiabetic miceLong-term potentiationCognitive impairmentPaired-pulse facilitationAutophagic inhibitionSynaptic plasticityAutophagic suppressionAnxiety-like behaviorCell deathDiabetes micePVT1 expressionHippocampal neuronsPresynaptic functionDiabetesTerm potentiationCell death analysisMiceSpatial learningImpairmentDeath analysisApoptotic cell deathDepotentiationInhibitionDeathPVT1
2015
Conditional overexpression of TGFβ1 promotes pulmonary inflammation, apoptosis and mortality via TGFβR2 in the developing mouse lung
Sureshbabu A, Syed MA, Boddupalli CS, Dhodapkar MV, Homer RJ, Minoo P, Bhandari V. Conditional overexpression of TGFβ1 promotes pulmonary inflammation, apoptosis and mortality via TGFβR2 in the developing mouse lung. Respiratory Research 2015, 16: 4. PMID: 25591994, PMCID: PMC4307226, DOI: 10.1186/s12931-014-0162-6.Peer-Reviewed Original ResearchMeSH KeywordsAcute Lung InjuryAlveolar Epithelial CellsAnimalsAnimals, NewbornApoptosisDisease Models, AnimalGenotypeHumansHyperoxiaLungMice, Inbred C57BLMice, KnockoutMice, TransgenicPhenotypePneumoniaProtein Serine-Threonine KinasesReceptor, Transforming Growth Factor-beta Type IIReceptors, Transforming Growth Factor betaSignal TransductionTime FactorsTransforming Growth Factor beta1Up-RegulationConceptsImpaired alveolarizationBronchopulmonary dysplasiaAlveolar epithelial cellsPulmonary inflammationPulmonary phenotypeMouse lungAcute lung injuryType II alveolar epithelial cellsApoptotic cell deathCell deathNewborn mouse lungPotential therapeutic strategyGrowth factor betaNull mutant miceLung injuryImproved survivalNeonatal mortalityMonocyte infiltrationAbnormal alveolarizationAngiogenic mediatorsInflammatory signalsTGFβ1 expressionTherapeutic strategiesInflammatory macrophagesLung morphometry
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