2022
CD38 Mediates Lung Fibrosis by Promoting Alveolar Epithelial Cell Aging.
Cui H, Xie N, Banerjee S, Dey T, Liu RM, Antony VB, Sanders YY, Adams TS, Gomez JL, Thannickal VJ, Kaminski N, Liu G. CD38 Mediates Lung Fibrosis by Promoting Alveolar Epithelial Cell Aging. American Journal Of Respiratory And Critical Care Medicine 2022, 206: 459-475. PMID: 35687485, DOI: 10.1164/rccm.202109-2151oc.Peer-Reviewed Original ResearchMeSH KeywordsAgingAlveolar Epithelial CellsAnimalsBleomycinCellular SenescenceHumansIdiopathic Pulmonary FibrosisLungMiceNADConceptsIdiopathic pulmonary fibrosisLung fibrosisCD38 expressionAlveolar epithelial cell injuryEpithelial cell injuryEffective therapeutic strategyHuman lung parenchymaIPF lungsLung functionPulmonary fibrosisDisease progressionFibrotic lungsReal-time PCRYoung miceLung parenchymaOld miceCell injuryTherapeutic strategiesFibrosisPharmacological inactivationCD38Single-cell RNA sequencingFlow cytometryWestern blottingOld animals
2021
Inhibition of PDIA3 in club cells attenuates osteopontin production and lung fibrosis
Kumar A, Elko E, Bruno SR, Mark ZF, Chamberlain N, Mihavics BK, Chandrasekaran R, Walzer J, Ruban M, Gold C, Lam YW, Ghandikota S, Jegga AG, Gomez JL, Janssen-Heininger YM, Anathy V. Inhibition of PDIA3 in club cells attenuates osteopontin production and lung fibrosis. Thorax 2021, 77: 669-678. PMID: 34400514, PMCID: PMC8847543, DOI: 10.1136/thoraxjnl-2021-216882.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBleomycinEpithelial CellsHumansIdiopathic Pulmonary FibrosisLungMiceOsteopontinProtein Disulfide-IsomerasesConceptsIdiopathic pulmonary fibrosisProtein disulfide isomerase A3Lung fibrosisPulmonary fibrosisClub cellsFibrosis-related proteinsMechanism of actionControl patientsLung functionBleomycin modelLung parenchymaFibrosisTherapeutic potentialMiceOsteopontin productionSpecific deletionPatientsProtein signaturesInhibitionResearch ConsortiumPathologyCellsSPP1Human transcriptome datasetsMajor interactors
2018
Reducing protein oxidation reverses lung fibrosis
Anathy V, Lahue KG, Chapman DG, Chia SB, Casey DT, Aboushousha R, van der Velden JLJ, Elko E, Hoffman SM, McMillan DH, Jones JT, Nolin JD, Abdalla S, Schneider R, Seward DJ, Roberson EC, Liptak MD, Cousins ME, Butnor KJ, Taatjes DJ, Budd RC, Irvin CG, Ho YS, Hakem R, Brown KK, Matsui R, Bachschmid MM, Gomez JL, Kaminski N, van der Vliet A, Janssen-Heininger YMW. Reducing protein oxidation reverses lung fibrosis. Nature Medicine 2018, 24: 1128-1135. PMID: 29988126, PMCID: PMC6204256, DOI: 10.1038/s41591-018-0090-y.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsFemaleGlutaredoxinsGlutathioneIdiopathic Pulmonary FibrosisLungMice, Inbred C57BLMice, TransgenicOxidation-ReductionProteinsConceptsIdiopathic pulmonary fibrosisPulmonary fibrosisLung fibrosisDirect administrationAirways of miceGrowth factor beta 1Transgenic mouse modelFibrotic lungsLung tissueMouse modelAged animalsFibrosisLung epitheliumTherapeutic potentialExcessive depositionBeta 1Transgenic overexpressionOxidative stressExact mechanismAirwayGlrxLungMiceAdministrationOxidative mechanisms