Featured Publications
Airway basal cells show a dedifferentiated KRT17highPhenotype and promote fibrosis in idiopathic pulmonary fibrosis
Jaeger B, Schupp JC, Plappert L, Terwolbeck O, Artysh N, Kayser G, Engelhard P, Adams TS, Zweigerdt R, Kempf H, Lienenklaus S, Garrels W, Nazarenko I, Jonigk D, Wygrecka M, Klatt D, Schambach A, Kaminski N, Prasse A. Airway basal cells show a dedifferentiated KRT17highPhenotype and promote fibrosis in idiopathic pulmonary fibrosis. Nature Communications 2022, 13: 5637. PMID: 36163190, PMCID: PMC9513076, DOI: 10.1038/s41467-022-33193-0.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisAirway basal cellsPulmonary fibrosisNovel mouse xenograft modelEffect of saracatinibBasal cellsLimited treatment optionsMouse xenograft modelLung developmental processesConnectivity Map analysisExtracellular matrix depositionIPF lungsBronchial brushSevere fibrosisTreatment optionsBronchial brushingsNRG miceHealthy volunteersXenograft modelCyst-like structuresProfibrotic changesAlveolar compartmentFatal diseaseFibrosisPotent Src inhibitormicroRNA-33 deficiency in macrophages enhances autophagy, improves mitochondrial homeostasis, and protects against lung fibrosis
Ahangari F, Price N, Malik S, Chioccioli M, Bärnthaler T, Adams T, Kim J, Pradeep S, Ding S, Cosme C, Rose K, McDonough J, Aurelien N, Ibarra G, Omote N, Schupp J, DeIuliis G, Nunez J, Sharma L, Ryu C, Dela Cruz C, Liu X, Prasse A, Rosas I, Bahal R, Fernandez-Hernando C, Kaminski N. microRNA-33 deficiency in macrophages enhances autophagy, improves mitochondrial homeostasis, and protects against lung fibrosis. JCI Insight 2023, 8: e158100. PMID: 36626225, PMCID: PMC9977502, DOI: 10.1172/jci.insight.158100.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisPulmonary fibrosisMiR-33MiR-33 levelsSpecific genetic ablationBronchoalveolar lavage cellsNovel therapeutic approachesMitochondrial homeostasisFatty acid metabolismMacrophages protectsBleomycin injuryLavage cellsLung fibrosisHealthy controlsInflammatory responseTherapeutic approachesImmunometabolic responsesCholesterol effluxFibrosisFatal diseasePharmacological inhibitionSterol regulatory element-binding protein (SREBP) genesGenetic ablationMacrophagesEx vivo mouse
2019
BAL Cell Gene Expression Is Indicative of Outcome and Airway Basal Cell Involvement in Idiopathic Pulmonary Fibrosis
Prasse A, Binder H, Schupp JC, Kayser G, Bargagli E, Jaeger B, Hess M, Rittinghausen S, Vuga L, Lynn H, Violette S, Jung B, Quast K, Vanaudenaerde B, Xu Y, Hohlfeld JM, Krug N, Herazo-Maya JD, Rottoli P, Wuyts WA, Kaminski N. BAL Cell Gene Expression Is Indicative of Outcome and Airway Basal Cell Involvement in Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2019, 199: 622-630. PMID: 30141961, PMCID: PMC6396865, DOI: 10.1164/rccm.201712-2551oc.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisAirway basal cellsChronic obstructive pulmonary diseaseObstructive pulmonary diseasePulmonary diseaseBAL cellsBasal cellsPulmonary fibrosisControl subjectsCell gene expressionIndependent IPF cohortsNine-gene signatureIPF cohortDerivation cohortClinical parametersRetrospective studyUnivariate analysisUnpredictable courseCell involvementDiscovery cohortGene expressionHealthy volunteersCox modelStage IIIFatal disease
2016
Right atrial pressure/pulmonary artery wedge pressure ratio: A more specific predictor of survival in pulmonary arterial hypertension
Fares WH, Bellumkonda L, Tonelli AR, Carson SS, Hassoun PM, Trow TK, Herzog EL, Kaminski N, Kholdani CA, Zhang L, Zhou Y, Hammel JP, Dweik RA. Right atrial pressure/pulmonary artery wedge pressure ratio: A more specific predictor of survival in pulmonary arterial hypertension. The Journal Of Heart And Lung Transplantation 2016, 35: 760-767. PMID: 26856665, DOI: 10.1016/j.healun.2015.12.028.Peer-Reviewed Original ResearchConceptsPulmonary arterial hypertensionHemodynamic variablesArterial hypertensionCohort 2Cohort 1Accurate prognostic variableRelative prognostic valueSpecific predictorsCurrent prognostic modelsMultivariable regression modelsPAH registryPAH patientsHazard ratioPAH cohortReferral centerPrognostic valueMean ageClinical trialsClinical prognosticationPrognostic variablesSeparate cohortDisease statusFatal diseasePrognostic modelSecondary analysis
2008
Transgelin is a direct target of TGF‐β/Smad3‐dependent epithelial cell migration in lung fibrosis
Yu H, Königshoff M, Jayachandran A, Handley D, Seeger W, Kaminski N, Eickelberg O. Transgelin is a direct target of TGF‐β/Smad3‐dependent epithelial cell migration in lung fibrosis. The FASEB Journal 2008, 22: 1778-1789. PMID: 18245174, DOI: 10.1096/fj.07-083857.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisReverse transcription-polymerase chain reactionLung fibrosisATII cellsPulmonary fibrosisType II cell hyperplasiaExcessive extracellular matrix depositionATII cell phenotypeCell phenotypeTranscription-polymerase chain reactionLung epithelial A549 cellsPrimary ATII cellsActivin-like kinase 5Epithelial A549 cellsTGF-beta treatmentExtracellular matrix depositionTransgelin geneIPF patientsTGF-beta signalingCell hyperplasiaTGF-beta target genesCell injuryLung specimenFibrosisFatal disease