Adjunct Faculty
Adjunct faculty typically have an academic or research appointment at another institution and contribute or collaborate with one or more School of Medicine faculty members or programs.
Adjunct rank detailsAurélien Justet
Assistant Professor AdjunctAbout
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Titles
Assistant Professor Adjunct
Appointments
Pulmonary, Critical Care & Sleep Medicine
Assistant Professor AdjunctPrimary
Other Departments & Organizations
Research
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Research at a Glance
Yale Co-Authors
Frequent collaborators of Aurélien Justet's published research.
Publications Timeline
A big-picture view of Aurélien Justet's research output by year.
Naftali Kaminski, MD
Taylor Adams
Farida Ahangari, MD
Xiting Yan, PhD
Jonas Christian Schupp, MD
Johad Khoury
114Publications
1,171Citations
Publications
2025
Inhibition of epithelial cell YAP-TEAD/LOX signaling attenuates pulmonary fibrosis in preclinical models
Wagner D, Alsafadi H, Mitash N, Justet A, Hu Q, Pineda R, Staab-Weijnitz C, Korfei M, Gvazava N, Wannemo K, Onwuka U, Mozurak M, Estrada-Bernal A, Cala-Garcia J, Mutze K, Costa R, Bölükbas D, Stegmayr J, Skronska-Wasek W, Klee S, Ota C, Baarsma H, Wang J, Sembrat J, Hilgendorff A, Ding J, Günther A, Chambers R, Rosas I, de Langhe S, Kaminski N, Lehmann M, Eickelberg O, Königshoff M. Inhibition of epithelial cell YAP-TEAD/LOX signaling attenuates pulmonary fibrosis in preclinical models. Nature Communications 2025, 16: 7099. PMID: 40753090, PMCID: PMC12318044, DOI: 10.1038/s41467-025-61795-x.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAdaptor Proteins, Signal TransducingAlveolar Epithelial CellsAnimalsCell Cycle ProteinsDisease Models, AnimalDNA-Binding ProteinsExtracellular MatrixFemaleHumansIdiopathic Pulmonary FibrosisLungMaleMiceMice, Inbred C57BLProtein-Lysine 6-OxidaseSignal TransductionTranscription FactorsVerteporfinYAP-Signaling ProteinsConceptsIdiopathic pulmonary fibrosisAlveolar typePulmonary fibrosisIdiopathic pulmonary fibrosis patientsAlveolar type II cellsFibrosis in vivoLung fibrosis in vivoExcessive extracellular matrix depositionType II cellsExcessive extracellular matrix productionPreclinical modelsExtracellular matrix depositionDisease progressionPotential therapiesTissue ex vivoYAP inhibitionCrosslinking of extracellular matrixII cellsLethal diseaseExtracellular matrix productionActive YAPFibrosisMatrix depositionInhibitionDiseaseA deep generative model for deciphering cellular dynamics and in silico drug discovery in complex diseases
Zheng Y, Schupp J, Adams T, Clair G, Justet A, Ahangari F, Yan X, Hansen P, Carlon M, Cortesi E, Vermant M, Vos R, De Sadeleer L, Rosas I, Pineda R, Sembrat J, Königshoff M, McDonough J, Vanaudenaerde B, Wuyts W, Kaminski N, Ding J. A deep generative model for deciphering cellular dynamics and in silico drug discovery in complex diseases. Nature Biomedical Engineering 2025, 1-26. PMID: 40542107, DOI: 10.1038/s41551-025-01423-7.Peer-Reviewed Original ResearchCitationsAltmetricConceptsComplex cellular dynamicsCellular dynamicsSingle-cell transcriptomic dataIn silico drug discoverySingle-cell transcriptomicsTranscriptome dataPotential therapeutic drug candidateComplex diseasesHuman diseasesIdiopathic pulmonary fibrosisTherapeutic drug candidateCell embeddingDrug discoveryPulmonary fibrosisDrug candidatesDisease progressionHuman tissuesHuman precision-cut lung slicesDynamic analysisPrecision-cut lung slicesPathological landscapeComputational toolsAnti-fibrotic effectsUnagiTranscriptomeUnderstanding and Reducing Cardiopulmonary Sequelae Associated With Chronic Hypoxia
Manning E, Ramachandra A, Sharma P, Nikola F, De Man R, Doddaballapur P, Raredon M, Szafron J, Baernthaler T, Justet A, Akingbesote N, Perry R, Adams T, Cavinato C, Yan X, Tellides G, Kaminski N, Humphrey J. Understanding and Reducing Cardiopulmonary Sequelae Associated With Chronic Hypoxia. American Journal Of Respiratory And Critical Care Medicine 2025, 211: a3336-a3336. DOI: 10.1164/ajrccm.2025.211.abstracts.a3336.Peer-Reviewed Original ResearchThe Potential Role of miR205 and miR205HG in Pulmonary Fibrosis
Anderson S, Johad K, Ahangari F, Justet A, Adams T, Yan X, Kaminski N. The Potential Role of miR205 and miR205HG in Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2025, 211: a4662-a4662. DOI: 10.1164/ajrccm.2025.211.abstracts.a4662.Peer-Reviewed Original ResearchThe PPFE Cell Atlas - The Discovery of the Usual Fibrotic Niche at the Edge of Pleuro-Parenchymal Fibroelastotic Remodeling Surprises as an Immune Cell Driven Phenomenon
Ruwisch J, Cazes A, leiber L, Borie R, Leonhard C, Mal H, Langer L, de Montpréville V, Kamp J, Greer M, Wrede C, Hegermann J, Artysh N, Gottlieb J, Seeliger B, Bernaudin J, Knudsen L, Mordant P, Neubert L, Crestani B, Prasse A, Kaminski N, Justet A, Schupp J. The PPFE Cell Atlas - The Discovery of the Usual Fibrotic Niche at the Edge of Pleuro-Parenchymal Fibroelastotic Remodeling Surprises as an Immune Cell Driven Phenomenon. American Journal Of Respiratory And Critical Care Medicine 2025, 211: a5272-a5272. DOI: 10.1164/ajrccm.2025.211.abstracts.a5272.Peer-Reviewed Original ResearchAltmetricConceptsEarly IPF Is Characterized by a Dramatic Shift of the Epithelial and Endothelial Populations Within the Alveolar Niche
Justet A, Adams T, Khoury J, Balayev A, Abu Hussein N, Schupp J, Zhao A, Manning E, Ahangari F, Yan X, Ravaglia C, Tomassetti S, Poletti V, Kaminski N. Early IPF Is Characterized by a Dramatic Shift of the Epithelial and Endothelial Populations Within the Alveolar Niche. American Journal Of Respiratory And Critical Care Medicine 2025, 211: a7109-a7109. DOI: 10.1164/ajrccm.2025.211.abstracts.a7109.Peer-Reviewed Original ResearchThe Potential Role of GPR87 in the Development of Pulmonary Fibrosis
Khoury J, Ahangari F, Justet A, Adams T, Manning E, Mcdonough J, Anderson S, Nekola F, Beermann M, Bauer Y, Gomez J, Kaminski N. The Potential Role of GPR87 in the Development of Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2025, 211: a7110-a7110. DOI: 10.1164/ajrccm.2025.211.abstracts.a7110.Peer-Reviewed Original ResearchRadiation toxicity and survival in patients with interstitial lung disease and non-small cell lung cancer: A case control study
Justet A, Jackson L, Bardon M, Lerouge D, Césaire M, Loiseau C, Bergot E, Christy F, Thariat J. Radiation toxicity and survival in patients with interstitial lung disease and non-small cell lung cancer: A case control study. Cancer/Radiothérapie 2025, 29: 104622. PMID: 40311519, DOI: 10.1016/j.canrad.2025.104622.Peer-Reviewed Original ResearchAltmetricMeSH Keywords and ConceptsConceptsInterstitial lung diseaseNon-small cell lung cancerProgression-free survivalCell lung cancerOverall survivalLung diseaseCase-control studyLung cancerCentral reviewOligometastatic non-small cell lung cancerMedian progression-free survivalCase-control study of patientsPrevalence of interstitial lung diseaseConsecutive lung cancer patientsIntensity-modulated radiotherapyStereotactic body radiotherapyMedian overall survivalThree-dimensional radiotherapyScore of fibrosisPrognosis of patientsGround-glass patternInterstitial pulmonary fibrosisStudy of patientsLung cancer patientsCancer treatment characteristicsApplying single cell profiling to assess drug anti fibrotic properties in the human precision cut lung slice model of fibrosis
Justet A, Mitash N, Pineda R, Adams T, Balayev A, Abu Hussein N, Ishizuka M, Kim H, Khoury J, Cala-García J, Ahangari F, Yan X, Kaminski N, Königshoff M. Applying single cell profiling to assess drug anti fibrotic properties in the human precision cut lung slice model of fibrosis. Revue Des Maladies Respiratoires 2025, 42: 223. DOI: 10.1016/j.rmr.2025.02.083.Peer-Reviewed Original ResearchConceptsAbnormal cell populationsAlveolar epithelial cellsTreated with drugsAnti-fibrotic propertiesSingle cell platformsSingle nuclear RNA sequencingLigand-receptor analysisPreclinical evidencePulmonary fibrosisBasaloid cellsFibrotic propertiesReceptor analysisFibrotic pathwaysCell signaturesClinical trialsProfibrotic genesAnti-fibroticFDA-approved drugsGene signatureAnimal modelsEpithelial cellsGene expression changesDay 5Drug efficacyCell profilesFGF21 Signaling Exerts Antifibrotic Properties during Pulmonary Fibrosis.
Ghanem M, Archer G, Justet A, Jaillet M, Vasarmidi E, Mordant P, Castier Y, Mal H, Cazes A, Poté N, Crestani B, Mailleux A. FGF21 Signaling Exerts Antifibrotic Properties during Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2025, 211: 486-498. PMID: 39637324, DOI: 10.1164/rccm.202311-2021oc.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsIdiopathic pulmonary fibrosisWild-type littermatesPlasma of patientsPulmonary fibrosisAntifibrotic propertiesIntratracheal injection of bleomycinDevelopment of pulmonary fibrosisDecreased fibrosis markersEffects of FGF21Increased sensitivity to bleomycinInjection of bleomycinPulmonary fibrosis developmentSensitivity to bleomycinDecrease of BaxConcentrations of FGF21Human lung fibroblastsTherapeutic optionsFibrosis markersAntifibrotic effectsControl subjectsInjury scoreIntratracheal injectionLiver fibrosisLung fibrogenesisFibroblast growth factor
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