2024
Succinate dehydrogenase–complex II regulates skeletal muscle cellular respiration and contractility but not muscle mass in genetically induced pulmonary emphysema
Balnis J, Tufts A, Jackson E, Drake L, Singer D, Lacomis D, Lee C, Elias J, Doles J, Maher L, Jen A, Coon J, Jourd’heuil D, Singer H, Vincent C, Jaitovich A. Succinate dehydrogenase–complex II regulates skeletal muscle cellular respiration and contractility but not muscle mass in genetically induced pulmonary emphysema. Science Advances 2024, 10: eado8549. PMID: 39167644, PMCID: PMC11338223, DOI: 10.1126/sciadv.ado8549.Peer-Reviewed Original ResearchConceptsPulmonary emphysemaMuscle massSuccinate dehydrogenaseReduced skeletal muscle massAssociated with high mortalityCellular respirationSkeletal muscle massReduced cellular respirationKnockout miceMuscle dysfunctionActivity of succinate dehydrogenaseComplex I respirationMitochondrial oxygen consumptionMyopathic changesTransgenic miceSubunit cMuscle atrophyProteomic effectsMyofiber contractilityRespirometry analysisSuccinate accumulationMuscle mitochondriaEmphysemaHigher mortalityAnimal data
2014
Cathepsin E Promotes Pulmonary Emphysema via Mitochondrial Fission
Zhang X, Shan P, Homer R, Zhang Y, Petrache I, Mannam P, Lee PJ. Cathepsin E Promotes Pulmonary Emphysema via Mitochondrial Fission. American Journal Of Pathology 2014, 184: 2730-2741. PMID: 25239563, PMCID: PMC4188869, DOI: 10.1016/j.ajpath.2014.06.017.Peer-Reviewed Original ResearchConceptsActivation/apoptosisPulmonary emphysemaChronic obstructive pulmonary disease (COPD) lungsCigarette smoke-induced lung diseaseSmoke-induced lung diseaseChronic obstructive pulmonary diseaseDynamin-related protein 1Obstructive pulmonary diseaseProtein 1Mitochondrial fission protein dynamin-related protein 1Lung tissue sectionsCathepsin ENew therapeutic targetsAir space enlargementFission protein dynamin-related protein 1Pulmonary diseaseEmphysematous changesClinical entityLung diseaseMolecular mechanismsEmphysema developmentMitochondrial fissionLung parenchymaE miceLung elasticity
2012
Retinoic Acid–related Orphan Receptor-α Is Induced in the Setting of DNA Damage and Promotes Pulmonary Emphysema
Shi Y, Cao J, Gao J, Zheng L, Goodwin A, An CH, Patel A, Lee JS, Duncan SR, Kaminski N, Pandit KV, Rosas IO, Choi AM, Morse D. Retinoic Acid–related Orphan Receptor-α Is Induced in the Setting of DNA Damage and Promotes Pulmonary Emphysema. American Journal Of Respiratory And Critical Care Medicine 2012, 186: 412-419. PMID: 22744720, PMCID: PMC5450975, DOI: 10.1164/rccm.201111-2023oc.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBiomarkersCells, CulturedDisease Models, AnimalDNA DamageDNA RepairGene Expression ProfilingHumansLungMiceMice, Inbred C57BLMice, Neurologic MutantsNuclear Receptor Subfamily 1, Group F, Member 1Oligonucleotide Array Sequence AnalysisPulmonary Disease, Chronic ObstructivePulmonary EmphysemaTobacco Smoke PollutionConceptsRetinoic acid-related orphan receptorAcid-related orphan receptorCigarette smoke extractLungs of patientsPathogenesis of emphysemaRORA expressionCigarette smokeAirspace enlargementSmoke extractCigarette smoke exposureSmoke-induced emphysemaOrphan receptorDNA damageActive smokingLung transplantationSmoke exposureLung cancerPulmonary emphysemaLung tissueEmphysemaPatientsGene expression profilingApoptotic cell deathMiceEnhanced susceptibility
2007
IL-18 Is Induced and IL-18 Receptor α Plays a Critical Role in the Pathogenesis of Cigarette Smoke-Induced Pulmonary Emphysema and Inflammation
Kang MJ, Homer RJ, Gallo A, Lee CG, Crothers KA, Cho SJ, Rochester C, Cain H, Chupp G, Yoon HJ, Elias JA. IL-18 Is Induced and IL-18 Receptor α Plays a Critical Role in the Pathogenesis of Cigarette Smoke-Induced Pulmonary Emphysema and Inflammation. The Journal Of Immunology 2007, 178: 1948-1959. PMID: 17237446, DOI: 10.4049/jimmunol.178.3.1948.Peer-Reviewed Original ResearchConceptsChronic obstructive lung diseaseObstructive lung diseaseIL-18Wild-type miceCigarette smokeLung diseasePulmonary emphysemaIL-18RalphaPathogenesis of CSEffects of CSAir-exposed miceIL-18 pathwayIL-18 receptor αIL-18R signalingTh1 inflammationPulmonary macrophagesEpithelial apoptosisReceptor αInflammationPotent stimulatorEmphysemaCaspase-1MiceCritical roleElevated levels
2006
Toll-like receptor 4 deficiency causes pulmonary emphysema
Zhang X, Shan P, Jiang G, Cohn L, Lee PJ. Toll-like receptor 4 deficiency causes pulmonary emphysema. Journal Of Clinical Investigation 2006, 116: 3050-3059. PMID: 17053835, PMCID: PMC1616193, DOI: 10.1172/jci28139.Peer-Reviewed Original ResearchConceptsToll-like receptor 4 deficiencyEndothelial cellsOxidant generationLung structural cellsAdoptive transfer experimentsNormal lung architectureDevelopment of emphysemaTLR4 deficiencyTLR4 expressionAirspace enlargementLung diseaseLung architecturePulmonary emphysemaLung integrityCigarette smokeLung elasticityEmphysemaNADPH inhibitorStructural cellsLungNovel NADPH oxidaseNADPH oxidaseElastolytic activityTLRMice
2003
Loss of integrin αvβ6-mediated TGF-β activation causes Mmp12-dependent emphysema
Morris DG, Huang X, Kaminski N, Wang Y, Shapiro SD, Dolganov G, Glick A, Sheppard D. Loss of integrin αvβ6-mediated TGF-β activation causes Mmp12-dependent emphysema. Nature 2003, 422: 169-173. PMID: 12634787, DOI: 10.1038/nature01413.Peer-Reviewed Original ResearchConceptsTGF-β activationLungs of miceActive TGF-β1Pulmonary gene expressionHeterodimeric cell-surface proteinsTransgenic expressionPulmonary emphysemaMMP12 expressionTGF-β1Functional alterationsΒ6 integrinIntegrin αvβ6Latent TGFMarked inductionEmphysemaGrowth factorMacrophage metalloelastaseCell surface proteinsActivation pathwayMiceTGFActivationCell growthIntegrinsExpression
2000
Interferon γ Induction of Pulmonary Emphysema in the Adult Murine Lung
Wang Z, Zheng T, Zhu Z, Homer R, Riese R, Chapman H, Shapiro S, Elias J. Interferon γ Induction of Pulmonary Emphysema in the Adult Murine Lung. Journal Of Experimental Medicine 2000, 192: 1587-1600. PMID: 11104801, PMCID: PMC2193095, DOI: 10.1084/jem.192.11.1587.Peer-Reviewed Original ResearchConceptsAdult murine lungMurine lungProtease/antiprotease balanceChronic obstructive pulmonary diseaseSecretory leukocyte proteinase inhibitorNeutrophil-rich inflammationObstructive pulmonary diseaseInterferon γ inductionPulmonary diseasePulmonary complianceChronic inflammationInflammatory responseLung volumePulmonary emphysemaPulmonary tissueΓ inductionAlveolar enlargementMMP-9Matrix metalloproteinaseEmphysemaLungInflammationSelective inhibitionProminent proteaseMacrophages
1999
Demonstration of Communication between Alveolus and Interstitium in Persistent Interstitial Pulmonary Emphysema: Case Report
Yao J, Fasano M, Morotti R, Caprio M, Greco M. Demonstration of Communication between Alveolus and Interstitium in Persistent Interstitial Pulmonary Emphysema: Case Report. Pediatric And Developmental Pathology 1999, 2: 484-487. PMID: 10441627, DOI: 10.1007/s100249900153.Peer-Reviewed Original ResearchConceptsPersistent interstitial pulmonary emphysemaInterstitial pulmonary emphysemaPulmonary emphysemaHyaline membrane diseaseAirway ruptureUncommon complicationPremature infantsMechanical ventilationMembrane diseaseCase reportImmunohistochemical stainsAlveolar levelPresumed mechanismDiseaseAirway systemInterstitiumEmphysema
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