Maurizio Chioccioli, PhD
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Appointments
Contact Info
About
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Assistant Professor of Comparative Medicine and of Genetics
Biography
Mau is an Assistant Professor in Genetics and Comparative Medicine at Yale School of Medicine. His research focus is to understand the molecular and cellular mechanisms that govern tissue regeneration and repair in the lung, and how these pathways are hijacked in disease. His experience and expertise span multiple areas from biophysics and live-imaging microscopy to molecular biology, genetics, and human respiratory diseases. Mau is from Arezzo, Tuscany. He obtained his undergraduate degree at the University of Florence in Tuscany, before going on to obtain his PhD from the Institute for Molecular Bioscience at the University of Queensland in Australia. He then performed his postdoctoral studies at the Cavendish Laboratory, Physics of Medicine Institute at Cambridge University where he worked on the biophysical basis of dynamic ciliary beating in respiratory diseases such as cystic fibrosis and primary ciliary dyskinesia. He was recruited into the lab of Naftali Kaminski at Yale School of Medicine in 2018 where he focused primarily on establishing new techniques and approaches to investigate lung remodeling and repair. He was appointed Assistant Professor in Genetics and Comparative Medicine in September 2023.
Appointments
Comparative Medicine
Assistant ProfessorFully JointGenetics
Assistant ProfessorFully JointPulmonary, Critical Care & Sleep Medicine
Assistant ProfessorSecondary
Other Departments & Organizations
- Comparative Medicine
- Genetics
- Internal Medicine
- Molecular Cell Biology, Genetics and Development
- Molecular Medicine, Pharmacology, and Physiology
- Pulmonary, Critical Care & Sleep Medicine
- Yale Combined Program in the Biological and Biomedical Sciences (BBS)
- Yale Stem Cell Center
Education & Training
- PhD
- University of Queensland, Molecular Biosciences
- MSc
- Universita Degli Studi Di Firenze, Molecular Biology (2007)
- BSc
- Universita Degli Studi Di Firenze, Biology (2004)
Research
Overview
Medical Research Interests
ORCID
0000-0003-2114-1825- View Lab Website
Chioccioli Lab
Research at a Glance
Yale Co-Authors
Publications Timeline
Research Interests
Naftali Kaminski, MD
Jonas Christian Schupp, MD
Farida Ahangari, MD
Maor Sauler, MD
Taylor Adams
Richard Pierce, MD
Alveolar Epithelial Cells
Publications
2024
A common polymorphism in the Intelectin-1 gene influences mucus plugging in severe asthma
Everman J, Sajuthi S, Liegeois M, Jackson N, Collet E, Peters M, Chioccioli M, Moore C, Patel B, Dyjack N, Powell R, Rios C, Montgomery M, Eng C, Elhawary J, Mak A, Hu D, Huntsman S, Salazar S, Feriani L, Fairbanks-Mahnke A, Zinnen G, Michel C, Gomez J, Zhang X, Medina V, Chu H, Cicuta P, Gordon E, Zeitlin P, Ortega V, Reisdorph N, Dunican E, Tang M, Elicker B, Henry T, Bleecker E, Castro M, Erzurum S, Israel E, Levy B, Mauger D, Meyers D, Sumino K, Gierada D, Hastie A, Moore W, Denlinger L, Jarjour N, Schiebler M, Wenzel S, Woodruff P, Rodriguez-Santana J, Pearson C, Burchard E, Fahy J, Seibold M. A common polymorphism in the Intelectin-1 gene influences mucus plugging in severe asthma. Nature Communications 2024, 15: 3900. PMID: 38724552, PMCID: PMC11082194, DOI: 10.1038/s41467-024-48034-5.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsAirway epithelial cellsIntelectin-1Mucus pluggingGene expressionAirways of severe asthmaticsEpithelial cellsHuman airway epithelial cellsAirway epithelial brushingsMucus secretory cellsT2-high asthmaFormation of mucus plugsAssociated with protectionC-terminusGenetic variantsAirway mucus pluggingMolecular roleSecretory cellsSecreted componentsEpithelial brushingsT2-lowIL-13Mucus obstructionTarget pathwaysSevere asthmaticsClinical significanceStem cell migration drives lung repair in living mice
Chioccioli M, Liu S, Magruder S, Tata A, Borriello L, McDonough J, Konkimalla A, Kim S, Nouws J, Gonzalez D, Traub B, Ye X, Yang T, Entenberg D, Krishnaswamy S, Hendry C, Kaminski N, Tata P, Sauler M. Stem cell migration drives lung repair in living mice. Developmental Cell 2024, 59: 830-840.e4. PMID: 38377991, PMCID: PMC11003834, DOI: 10.1016/j.devcel.2024.02.003.Peer-Reviewed Original ResearchCitationsAltmetricConceptsStem cell migrationCell migrationAlveolar type 2 cellsAlveolar unitsStem cell motilityAlveolar type 1 cellsStem cell activityCellular response to injuryResponse to injuryType 2 cellsMotile phenotypeType 1 cellsCell motilityLung repairImpaired regenerationGenetic depletionCell activationAT2Stem cellsTissue repairAT1Longitudinal imagingInjuryMotilityCellular resolution
2023
Alveolar Vascular Remodeling in Nonspecific Interstitial Pneumonia: Replacement of Normal Lung Capillaries with COL15A1-Positive Endothelial Cells.
Schupp J, Manning E, Chioccioli M, Kamp J, Christian L, Ryu C, Herzog E, Kühnel M, Prasse A, Kaminski N, Jonigk D, Homer R, Neubert L, Ius F, stringJustet A, Hariri L, Seeliger B, Welte T, Knipe R, Gottlieb J. Alveolar Vascular Remodeling in Nonspecific Interstitial Pneumonia: Replacement of Normal Lung Capillaries with COL15A1-Positive Endothelial Cells. American Journal Of Respiratory And Critical Care Medicine 2023, 208: 819-822. PMID: 37552025, PMCID: PMC10563189, DOI: 10.1164/rccm.202303-0544le.Peer-Reviewed Original ResearchCitationsAltmetricMicroRNA-1 protects the endothelium in acute lung injury
Korde A, Haslip M, Pednekar P, Khan A, Chioccioli M, Mehta S, Lopez-Giraldez F, Bermejo S, Rojas M, Dela Cruz C, Matthay M, Pober J, Pierce R, Takyar S. MicroRNA-1 protects the endothelium in acute lung injury. JCI Insight 2023, 8: e164816. PMID: 37737266, PMCID: PMC10561733, DOI: 10.1172/jci.insight.164816.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsAcute respiratory distress syndromeAcute lung injuryVascular endothelial growth factorAngiopoietin-2Lung injuryAcute injuryMiR-1MicroRNA-1Endothelial cell-specific overexpressionSevere endothelial dysfunctionRespiratory distress syndromeSurvival of miceIntrinsic protective effectContext of injuryCell-specific overexpressionEndothelial growth factorFamily member 3Pneumonia cohortMiR-1 targetsEndothelial dysfunctionDistress syndromeBarrier dysfunctionCapillary leakProtective effectSevere formMild Phenotypes in French-Canadians With TT25-related Primary Ciliary Dyskinesia
Palani M, Ding S, Ma K, Lek M, Vinh D, Henry M, Knowles M, Zariwala M, Leigh M, Chioccioli M, Shapiro A. Mild Phenotypes in French-Canadians With TT25-related Primary Ciliary Dyskinesia. 2023, a6109-a6109. DOI: 10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a6109.Peer-Reviewed Original ResearchmicroRNA-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 ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsIdiopathic 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 mousePhototaxis of Chlamydomonas arises from a tuned adaptive photoresponse shared with multicellular Volvocine green algae
Leptos K, Chioccioli M, Furlan S, Pesci A, Goldstein R. Phototaxis of Chlamydomonas arises from a tuned adaptive photoresponse shared with multicellular Volvocine green algae. Physical Review E 2023, 107: 014404. PMID: 36797913, PMCID: PMC7616094, DOI: 10.1103/physreve.107.014404.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsVolvocine algaeGreen algaeVolvocine green algaeMulticellular speciesMulticellular organismsEvolutionary transitionsChlamydomonasVolvoxAlgaeIndividual flagellaExtracellular matrixIndividual cellsIntercellular connectionsAdaptive responsePrimary axisGoniumSwimming cellsLight levelsPhototaxisOrganismsSpeciesFlagellar responsesCell numberCellsBeat plane
2022
Saracatinib, a Selective Src Kinase Inhibitor, Blocks Fibrotic Responses in Preclinical Models of Pulmonary Fibrosis.
Ahangari F, Becker C, Foster DG, Chioccioli M, Nelson M, Beke K, Wang X, Justet A, Adams T, Readhead B, Meador C, Correll K, Lili LN, Roybal HM, Rose KA, Ding S, Barnthaler T, Briones N, DeIuliis G, Schupp JC, Li Q, Omote N, Aschner Y, Sharma L, Kopf KW, Magnusson B, Hicks R, Backmark A, Dela Cruz CS, Rosas I, Cousens LP, Dudley JT, Kaminski N, Downey GP. Saracatinib, a Selective Src Kinase Inhibitor, Blocks Fibrotic Responses in Preclinical Models of Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2022, 206: 1463-1479. PMID: 35998281, PMCID: PMC9757097, DOI: 10.1164/rccm.202010-3832oc.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsIdiopathic pulmonary fibrosisHuman precision-cut lung slicesPrecision-cut lung slicesPulmonary fibrosisNormal human lung fibroblastsEpithelial-mesenchymal transitionHuman lung fibroblastsFibrogenic pathwaysPreclinical modelsMurine modelLung slicesSrc kinase inhibitorLung fibroblastsKinase inhibitorsAmelioration of fibrosisSelective Src kinase inhibitorHuman lung fibrosisWhole lung extractsPotential therapeutic efficacyIPF diseaseIPF treatmentLung functionInflammatory cascadeLung fibrosisAntifibrotic efficacyA lung targeted miR-29 mimic as a therapy for pulmonary fibrosis
Chioccioli M, Roy S, Newell R, Pestano L, Dickinson B, Rigby K, Herazo-Maya J, Jenkins G, Ian S, Saini G, Johnson SR, Braybrooke R, Yu G, Sauler M, Ahangari F, Ding S, DeIuliis J, Aurelien N, Montgomery RL, Kaminski N. A lung targeted miR-29 mimic as a therapy for pulmonary fibrosis. EBioMedicine 2022, 85: 104304. PMID: 36265417, PMCID: PMC9587275, DOI: 10.1016/j.ebiom.2022.104304.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsIdiopathic pulmonary fibrosisNon-human primatesPulmonary fibrosisAnimal modelsPro-fibrotic genesAnti-fibrotic efficacyMiR-29 mimicsHuman peripheral bloodMiR-29b levelsHuman lung fibroblastsIPF patientsIPF diagnosisPeripheral bloodReduced fibrosisAdverse findingsPotential therapyLung slicesTGF-β1Relevant dosesLung fibroblastsNIH-NHLBIFibrosisTherapyCollagen productionProfibrotic gene programMicroRNA-1 Regulates an Endothelial Gene Network Controlling Permeability and Alveolar Cell Death
Korde A, Haslip M, Chioccioli M, Khan A, Mehta S, Pober J, Pierce R, Takyar S. MicroRNA-1 Regulates an Endothelial Gene Network Controlling Permeability and Alveolar Cell Death. 2022, a5771-a5771. DOI: 10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a5771.Peer-Reviewed Original Research
Academic Achievements & Community Involvement
activity Postdoctoral Research Associate
ResearchDetails01/15/2015 - 01/15/2018Cambridge, England, United KingdomCollaborators- Prof Max SeiboldNJH, Denver CO
- Dr Preston BratcherNJH, Denver CO
- Prof Vito MennellaSickKids Hospital, University of Toronto, Canada
- Prof Sharon DellSickKids Hospital, University of Toronto, Canada
- Prof Israel AmiravUniversity of Alberta, Canada
Abstract/SynopsisThe Cavendish Laboratory - Physics of Medicine
activity Postdoctoral Research Associate
ResearchDetails03/08/2013 - 12/15/2014Cambridge, England, United KingdomAbstract/SynopsisDepartment of Applied Mathematics and Theoretical Physics
News
News
- July 09, 2024
Meet Maurizio Chioccioli and his research on lung injury repair
- February 21, 2024Source: YaleNews
Stem Cells ‘Migrate’ to Repair Damaged Lung Cells, Study Shows
- October 28, 2022
Newly Designed Molecule Is Promising Potential Therapy for Deadly Lung Condition
- April 18, 2019Source: Cystic Fibrosis News Today
New Test Could Lead to Effectively Customizing Treatments for CF Patients, Study Contends
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Locations
Brady Memorial Laboratory
Academic Office
310 Cedar Street, Fl 3, Rm 330C
New Haven, CT 06510
Brady Memorial Laboratory
Lab
310 Cedar Street, Fl 3, Rm 316, 316A
New Haven, CT 06510