Featured Publications
microRNA-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
2024
Anti-inflammatory roles of type I interferon signaling in the lung
Feng J, Liu Y, Kim J, Ahangari F, Kaminski N, Bain W, Jie Z, Dela Cruz C, Sharma L. Anti-inflammatory roles of type I interferon signaling in the lung. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2024, 326: l551-l561. PMID: 38375579, PMCID: PMC11380987, DOI: 10.1152/ajplung.00353.2023.Peer-Reviewed Original ResearchType I interferon signalingIfnar1-/- miceI interferon signalingInflammatory cell responseInflammatory responseIfnar1-/-Bleomycin injuryCell responsesWild-type miceBroncho-alveolar lavageElevated inflammatory responsePersistent inflammatory responseChemotherapeutic agent bleomycinAnti-inflammatory roleClinically relevant stimuliAnti-inflammatory mechanismsMyeloid cellsPersistent inflammationLung injuryFibrotic remodelingBacterial clearanceRIG-I signalingNOD-like receptor signalingLung tissueReceptor signaling
2020
Mitochondrial antiviral signaling protein is crucial for the development of pulmonary fibrosis
Kim SH, Lee JY, Yoon CM, Shin HJ, Lee SW, Rosas I, Herzog E, Dela Cruz C, Kaminski N, Kang MJ. Mitochondrial antiviral signaling protein is crucial for the development of pulmonary fibrosis. European Respiratory Journal 2020, 57: 2000652. PMID: 33093124, PMCID: PMC8559259, DOI: 10.1183/13993003.00652-2020.Peer-Reviewed Original ResearchConceptsDamage-associated molecular patternsIdiopathic pulmonary fibrosisPulmonary fibrosisMAVS aggregationMultiple damage-associated molecular patternsExperimental pulmonary fibrosisMitochondrial antiviral signaling proteinInnate immune responseIPF patientsMAVS signalingIPF treatmentBleomycin injuryLung fibrosisTherapeutic effectImmune responseTherapeutic strategiesMAVS expressionFibrosisDanger signalsCritical mediatorMolecular patternsABT-263LungInjuryBH3 mimetics
2016
Expression of RXFP1 Is Decreased in Idiopathic Pulmonary Fibrosis. Implications for Relaxin-based Therapies
Tan J, Tedrow JR, Dutta JA, Juan-Guardela B, Nouraie M, Chu Y, Trejo Bittar H, Ramani K, Biswas PS, Veraldi KL, Kaminski N, Zhang Y, Kass DJ. Expression of RXFP1 Is Decreased in Idiopathic Pulmonary Fibrosis. Implications for Relaxin-based Therapies. American Journal Of Respiratory And Critical Care Medicine 2016, 194: 1392-1402. PMID: 27310652, PMCID: PMC5148141, DOI: 10.1164/rccm.201509-1865oc.Peer-Reviewed Original ResearchConceptsRelaxin/insulin-like family peptide receptor 1Idiopathic pulmonary fibrosisIPF lung fibroblastsRXFP1 expressionLung fibroblastsPulmonary fibrosisFamily peptide receptor 1RXFP1 gene expressionLung Tissue Research ConsortiumPulmonary functionIPF lungsBleomycin injuryPotential therapyCollagen depositionFibrotic diseasesPatientsDemographic dataPotential efficacyReceptor 1Donor controlsTherapyRelaxin-like peptideGrowth factorGene expressionFibrosis
2012
Cytokine-Like Factor 1 Gene Expression Is Enriched in Idiopathic Pulmonary Fibrosis and Drives the Accumulation of CD4+ T Cells in Murine Lungs Evidence for an Antifibrotic Role in Bleomycin Injury
Kass DJ, Yu G, Loh KS, Savir A, Borczuk A, Kahloon R, Juan-Guardela B, Deiuliis G, Tedrow J, Choi J, Richards T, Kaminski N, Greenberg SM. Cytokine-Like Factor 1 Gene Expression Is Enriched in Idiopathic Pulmonary Fibrosis and Drives the Accumulation of CD4+ T Cells in Murine Lungs Evidence for an Antifibrotic Role in Bleomycin Injury. American Journal Of Pathology 2012, 180: 1963-1978. PMID: 22429962, PMCID: PMC3354590, DOI: 10.1016/j.ajpath.2012.01.010.Peer-Reviewed Original ResearchMeSH KeywordsAcute Lung InjuryAnimalsBleomycinCD4-Positive T-LymphocytesCiliary Neurotrophic Factor Receptor alpha SubunitCollagenDrug InteractionsEpithelial CellsGene Expression ProfilingHumansIdiopathic Pulmonary FibrosisMacrophages, AlveolarMaleMicePulmonary AlveoliRatsRats, Sprague-DawleyReceptors, CytokineRecombinant ProteinsRNA, MessengerUp-RegulationConceptsIdiopathic pulmonary fibrosisType II alveolar epithelial cellsCytokine receptor-like factor 1Alveolar epithelial cellsPulmonary fibrosisCardiotrophin-like cytokineCiliary neurotrophic factor receptorIPF lungsT cellsEpithelial cellsPathogenesis of IPFAccumulation of CD4IL-6 family membersExperimental pulmonary fibrosisFatal lung diseaseNeurotrophic factor receptorAntifibrotic responsesIPF pathogenesisT helperPulmonary accumulationBleomycin injuryInterleukin-6 familyLung diseaseAntifibrotic roleCytokine interferon
2011
Cytokine-Like Factor I (CLF1) Expression Is Increased In Idiopathic Pulmonary Fibrosis (IPF) And Promotes Inflammation But Decreases Fibrosis In Bleomycin Injury
Kass D, Loh K, Borczuk A, Tedrow J, Guardela B, Kaminski N, Greenberg S. Cytokine-Like Factor I (CLF1) Expression Is Increased In Idiopathic Pulmonary Fibrosis (IPF) And Promotes Inflammation But Decreases Fibrosis In Bleomycin Injury. 2011, a2710-a2710. DOI: 10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2710.Peer-Reviewed Original Research