2018
Time for a change: is idiopathic pulmonary fibrosis still idiopathic and only fibrotic?
Wolters PJ, Blackwell TS, Eickelberg O, Loyd JE, Kaminski N, Jenkins G, Maher TM, Molina-Molina M, Noble PW, Raghu G, Richeldi L, Schwarz MI, Selman M, Wuyts WA, Schwartz DA. Time for a change: is idiopathic pulmonary fibrosis still idiopathic and only fibrotic? The Lancet Respiratory Medicine 2018, 6: 154-160. PMID: 29413083, PMCID: PMC5903445, DOI: 10.1016/s2213-2600(18)30007-9.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisPulmonary fibrosisDevelopment of IPFFatal lung diseaseAlveolar epithelial cellsClinical presentationDistal airwaysLung diseaseFibroblast fociSubpleural fibrosisMicroscopic honeycombingPathogenic mechanismsFibrosisDiseaseEpithelial cellsMolecular mechanismsAirwayPathogenesisHoneycombingCentral driver
2017
Transcriptome profiles in sarcoidosis and their potential role in disease prediction
Schupp JC, Vukmirovic M, Kaminski N, Prasse A. Transcriptome profiles in sarcoidosis and their potential role in disease prediction. Current Opinion In Pulmonary Medicine 2017, 23: 487-492. PMID: 28590292, PMCID: PMC5637542, DOI: 10.1097/mcp.0000000000000403.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsGenome-wide expression studiesWide expression studiesTranscriptome profilesTranscriptomic dataRNA sequencingExpression studiesGene expressionMolecular mechanismsLarge prospective followTh1 immune responseTranscriptomeNonnecrotizing granulomasProspective followSystemic diseaseDisease progressionTreatment outcomesImmune responseSarcoidosisPotential roleControl tissuesProgressive sarcoidosisKey roleDiseaseTranscriptomicsGranulomas
2016
Integrated Genomics Reveals Convergent Transcriptomic Networks Underlying Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis
Kusko RL, Brothers JF, Tedrow J, Pandit K, Huleihel L, Perdomo C, Liu G, Juan-Guardela B, Kass D, Zhang S, Lenburg M, Martinez F, Quackenbush J, Sciurba F, Limper A, Geraci M, Yang I, Schwartz DA, Beane J, Spira A, Kaminski N. Integrated Genomics Reveals Convergent Transcriptomic Networks Underlying Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2016, 194: 948-960. PMID: 27104832, PMCID: PMC5067817, DOI: 10.1164/rccm.201510-2026oc.Peer-Reviewed Original ResearchMeSH KeywordsAdultEmphysemaFemaleGene Regulatory NetworksHumansHypoxia-Inducible Factor 1, alpha SubunitIdiopathic Pulmonary FibrosisI-kappa B ProteinsMaleMembrane ProteinsMiddle AgedNerve Tissue ProteinsOligonucleotide Array Sequence AnalysisPlatelet-Derived Growth FactorProto-Oncogene Proteins c-mdm2Pulmonary Disease, Chronic ObstructiveConceptsChronic obstructive pulmonary diseaseIdiopathic pulmonary fibrosisObstructive pulmonary diseasePulmonary diseasePulmonary fibrosisNCounter Analysis SystemHypoxia pathwayQuantitative polymerase chain reactionTranscriptomic pathwaysPolymerase chain reactionIndependent cohortEmphysemaIndependent sample setDiseaseGene expression arraysEnvironmental exposuresChain reactionFibrosisLungMolecular mechanismsExpression arraysMiR96Integrative genomics approachTranscriptional regulatory hubsPathway
2002
Gene expression analysis reveals matrilysin as a key regulator of pulmonary fibrosis in mice and humans
Zuo F, Kaminski N, Eugui E, Allard J, Yakhini Z, Ben-Dor A, Lollini L, Morris D, Kim Y, DeLustro B, Sheppard D, Pardo A, Selman M, Heller RA. Gene expression analysis reveals matrilysin as a key regulator of pulmonary fibrosis in mice and humans. Proceedings Of The National Academy Of Sciences Of The United States Of America 2002, 99: 6292-6297. PMID: 11983918, PMCID: PMC122942, DOI: 10.1073/pnas.092134099.Peer-Reviewed Original ResearchConceptsPulmonary fibrosisFibrotic lungsHuman pulmonary fibrosisPotential therapeutic targetGene expression analysisClinical diseaseSmooth muscleKnockout miceTherapeutic targetFibrosisHuman tissue samplesUntreatable groupLungTissue samplesMolecular pathwaysGlobal gene expression analysisExtracellular matrix formationMiceExpression analysisMatrilysinMolecular mechanismsKey regulatorGene expression patternsExpression patternsOligonucleotide microarrays
2000
Global analysis of gene expression in pulmonary fibrosis reveals distinct programs regulating lung inflammation and fibrosis
Kaminski N, Allard J, Pittet J, Zuo F, Griffiths M, Morris D, Huang X, Sheppard D, Heller R. Global analysis of gene expression in pulmonary fibrosis reveals distinct programs regulating lung inflammation and fibrosis. Proceedings Of The National Academy Of Sciences Of The United States Of America 2000, 97: 1778-1783. PMID: 10677534, PMCID: PMC26512, DOI: 10.1073/pnas.97.4.1778.Peer-Reviewed Original ResearchConceptsPulmonary fibrosisLung inflammationBleomycin administrationSusceptible miceMultiple time pointsFibrotic responseFibrosisFibrotic diseasesInflammationMore effective strategiesGene expressionTime pointsMiceBeta6 subunitMolecular mechanismsSequential inductionGene expression patternsExpression patternsNull mutationResponseEffective strategyLungExpressionBleomycinGene expression programs