Micha Sam Brickman Raredon, MD, PhD
Assistant Professor of AnesthesiologyCards
Appointments
Contact Info
Vascular Biology and Therapeutics Program
10 Amistad Street, Rm. 301A
New Haven, Connecticut 06519
United States
About
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Titles
Assistant Professor of Anesthesiology
Biography
Dr. Micha Sam Brickman Raredon is an Assistant Professor in the Department of Anesthesiology at the Yale School of Medicine. The Raredon Laboratory studies regenerative tissue engineering, with a particular focus on cell-to-cell communication networks, and builds primary-source software to explore and analyze these complex data, including NICHES and Connectome. Dr. Raredon's laboratory seeks to reverse-engineer tissues for regenerative medicine through the close study of tissue systems biology.
Dr. Raredon completed his MD/PhD training at Yale in the laboratory of Dr. Laura Niklason (Biomedical Engineering), co-mentored by Dr. Naftali Kaminski (Pulmonary, Critical Care & Sleep Medicine), Dr. Andre Levchenko (Systems Biology) and Dr. Yuval Kluger (Applied Math). In 2022 he founded his lab as an independent group leader under the mentorship of Dr. Kaminski, Dr. Ruslan Medzhitov (Immunobiology), and Dr. Robert Schonberger (Anesthesiology). Dr. Raredon is now an independent research faculty member of the Vascular Biology and Therapeutics Program at Yale and the Program in Translational Biomedicine.
Dr. Raredon received a master's degree in Materials Science and Engineering at the Massachusetts Institute of Technology, where he received the Draper Fellowship to develop vascular tissue micro-fabrication techniques in the laboratories of Dr. Linda Griffith (Bioengineering), Dr. Paula Hammond (Chemical Engineering), and Dr. Jeffrey Borenstein (Draper Labs). He completed his undergraduate work in Biomedical Engineering and the History of Art at Yale University and the University of Cambridge.
Dr. Raredon plays the cello and enjoys finding time to be outdoors and near water as much as possible.
Appointments
Anesthesiology
Assistant ProfessorPrimary
Other Departments & Organizations
- All Institutions
- Anesthesiology
- Janeway Society
- Molecular Medicine, Pharmacology, and Physiology
- Program in Translational Biomedicine (PTB)
- Vascular Biology and Therapeutics Program
- Yale Biomedical Imaging Institute
- Yale Combined Program in the Biological and Biomedical Sciences (BBS)
Education & Training
- Independent Group Leader, T32 Fellowship
- Yale School of Medicine (2024)
- MD
- Yale School of Medicine (2022)
- PhD
- Yale School of Engineering and Applied Science, Biomedical Engineering (2021)
- MS
- Yale School of Engineering and Applied Science, Biomedical Engineering (2020)
- MPhil
- Yale School of Engineering and Applied Science, Biomedical Engineering (2020)
- MS
- Massachusetts Institute of Technology, Materials Science and Engineering (2014)
- BS
- Yale University, Biomedical Engineering & History of Art (2011)
Research
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Overview
Dr. Raredon's research group focuses on the mechanisms governing the behavior of complex multicellular systems and in leveraging these principles to engineer living tissues for regenerative medicine. Our work combines systems biology, stem-cell engineering, materials science, surgical fabrication, and biological engineering. The team is particularly invested in engineering, or controlling the self-organization of, cross-length scale perfusable vascular networks and tissue architecture, and in devising principles of microvascular construction and control that can be applied across organ types. We are a clinically-integrated laboratory with two broadly interconnected goals: the modeling of network-level mechanisms of tissue morphogenesis and phenotype regulation, and the application of those models to the design and fabrication of patient-specific tissues for therapeutic use.
Medical Research Interests
ORCID
0000-0003-1441-6122- View Lab Website
Raredon Laboratory
Research at a Glance
Yale Co-Authors
Publications Timeline
Research Interests
Naftali Kaminski, MD
Taylor Adams
Allison M. Greaney, PhD
Jonas Christian Schupp, MD
Laura Niklason, PhD, MD
Xiting Yan, PhD
Tissue Engineering
Computational Biology
Publications
2026
Pulmonary organoid models demonstrate compositionally driven epithelial plasticity and immune polarization
Edelstein S, Mizoguchi S, Gracia M, Wang N, Lee V, Obata T, Kim H, Haynes C, Danelski C, Tsuchiya T, Sauler M, Raredon M. Pulmonary organoid models demonstrate compositionally driven epithelial plasticity and immune polarization. IScience 2026, 29: 115030. DOI: 10.1016/j.isci.2026.115030.Peer-Reviewed Original ResearchAltmetricConceptsChronic lung diseaseLung diseaseEpithelial plasticityOrganoid modelsMacrophage activation profilesImmune-regulatory genesIdiopathic pulmonary fibrosisChronic obstructive pulmonary diseaseObstructive pulmonary diseaseLung organoid modelImmune remodelingPulmonary fibrosisImmune coordinationEpithelial regenerationImmune polarizationEpithelial fateInflammatory responsePulmonary diseaseInflammatory signalingRegenerative outcomesTransitional cell stateTransitional cellsMacrophage polarizationRegenerative mechanismsDiseaseVascular Endothelial Growth Factor-D Improves Lung Vascular Integrity During Acute Lung Injury.
Yoon Y, Sharma L, Tang W, Kirk S, Raredon M, Ahangari F, Khoury J, Qian H, Ke Y, Tulapurkar M, Liu R, Luan Y, Yuan Q, Chen L, Birukov K, Simons M, Wu D, Niklason L, Kaminski N, Yuan Y. Vascular Endothelial Growth Factor-D Improves Lung Vascular Integrity During Acute Lung Injury. Circulation Research 2026 PMID: 41822962, PMCID: PMC13007730, DOI: 10.1161/circresaha.124.326094.Peer-Reviewed Original ResearchAltmetricConceptsVEGF-DAcute lung injuryBarrier-protective effectsVascular integrityLung injuryLipopolysaccharide-induced acute lung injury modelIntravenous administrationTNF-aParacrine signalingModel of acute lung injuryPulmonary vascular integrityLigand-receptor interactionsImmune cell infiltrationAcute lung injury modelLung vascular integrityVEGFR2-dependent signalingLung injury modelEndothelial barrier integrityEndothelial barrier functionRNA sequencing dataMicrovascular endothelial cellsInhibition of VEGFR2Microvascular nichePharmacological blockadeAssociated with pathwaysPulmonary Organoid Models Demonstrate Compositionally Driven Epithelial Plasticity and Immune Polarization
Edelstein SE, Mizoguchi S, Gracia MT, Wang N, Lee V, Obata T, Kim H, Haynes C, Danelski C, Tsuchiya T, Sauler M, Brickman Raredon MS. Pulmonary Organoid Models Demonstrate Compositionally Driven Epithelial Plasticity and Immune Polarization. IScience 2026, 115030. DOI: 10.1016/j.isci.2026.115030.Peer-Reviewed Original ResearchProximal Pulmonary Artery Stiffening as a Biomarker of Cardiopulmonary Aging
De Man R, Cai Z, Doddaballapur P, Guerrera N, Regan A, Lin L, Schwarz E, Justet A, Abu Hussein N, Di Palo J, Cavinato C, Raredon M, Heerdt P, Singh I, Yan X, Kang M, Bruns D, Lee P, Tellides G, Humphrey J, Kaminski N, Ramachandra A, Manning E. Proximal Pulmonary Artery Stiffening as a Biomarker of Cardiopulmonary Aging. Aging Cell 2026, 25: e70383. PMID: 41589414, PMCID: PMC12836046, DOI: 10.1111/acel.70383.Peer-Reviewed Original ResearchAltmetricMeSH Keywords and ConceptsConceptsProximal pulmonary arteriesPulmonary arterySmooth muscle cellsPerivascular macrophagesMouse modelMuscle cellsRight ventricle functionMedial smooth muscle cellsPulmonary arterial stiffeningRight ventricleVentricle functionAssociated with senescenceECM turnoverLung functionArterial stiffeningArteryAdventitial fibroblastsMolecular targetsAge-relatedGeroscience hypothesisLungAgeIntercellular signalingMiceMacrophagesEpithelial Reprogramming and Transition during Pulmonary Bioengineering.
Mizoguchi S, Lee V, Kim H, Edelstein SE, Wang N, Gracia MT, Danelski C, Haynes C, Rivero R, Stitelman D, Obata T, Greaney AM, Tsuchiya T, Kyriakides TR, Kaminski N, Raredon MSB. Epithelial Reprogramming and Transition during Pulmonary Bioengineering. BioRxiv 2026 PMID: 41659587, DOI: 10.64898/2026.01.24.701406.Peer-Reviewed Original ResearchAberrant cellular communities underlying disease heterogeneity in chronic obstructive pulmonary disease
Zhang Y, Wei H, Nouws J, Jiang W, Brewster R, Nguyen J, Liang S, Pass S, Wang W, Collin F, Oill A, Kim S, Siller S, Liu J, Zhao A, Hansbro P, Dela Cruz C, Britto C, Gomez J, Cloonan S, Herzog E, Lam T, Banovich N, Raredon M, Zhang X, Mangiola S, Homer R, Kaminski N, McDonough J, Polverino F, Yan X, Sauler M. Aberrant cellular communities underlying disease heterogeneity in chronic obstructive pulmonary disease. Nature Genetics 2026, 58: 376-391. PMID: 41578022, PMCID: PMC12900648, DOI: 10.1038/s41588-025-02480-z.Peer-Reviewed Original ResearchAltmetricMeSH Keywords and ConceptsConceptsChronic obstructive pulmonary diseaseObstructive pulmonary diseasePlasma biomarkersPulmonary diseaseComposite symptom scoreStudy participantsCell statesEarly COPDCellular landscapeNonimmune cellsCell communication analysisSymptom scoresImmune populationsSingle-nucleus RNA sequencingDisease progressionTherapeutic strategiesLung functionLung tissueChronic obstructive pulmonary disease heterogeneityMolecular driversDisease heterogeneityRegenerative stateCell compositionPathological cellsCell-autonomousSingle-cell atlas of human lung aging identifies cell type dyssynchrony and increased transcriptional entropy
De Man R, McDonough J, Adams T, Nikola F, Rangel R, Anderson S, Manning E, Cala Garcia J, Moss B, Waich A, Poli F, Cardenas R, Coarfa C, Song Q, Bar-Joseph Z, Vanaudenaerde B, Wuyts W, Niklason L, Raredon M, Yan X, Rosas I, Kaminski N. Single-cell atlas of human lung aging identifies cell type dyssynchrony and increased transcriptional entropy. Nature Communications 2026, 17: 2095. PMID: 41571679, PMCID: PMC12953888, DOI: 10.1038/s41467-026-68810-9.Peer-Reviewed Original ResearchAltmetricMeSH Keywords and ConceptsConceptsGenomic landscapeLung ageSingle-cell atlasAlveolar epithelialIndependent predictorsAnalysis of somatic mutationsSingle-cell dataSingle-cell RNA sequencingEndothelial cellsLoss of differentiationAlveolar epithelial cellsRNA sequencingTranscriptional changesCell-typeEndothelial cell typesSomatic mutationsMutational burdenAT2 cellsLung diseaseCell typesAge-related changesEpithelial cellsRisk factorsSenescence signatureEpithelial
2025
TSP2 Deficiency Promotes Fibroblast Proliferation and Migration With Enhanced WNT4/β‐Catenin/TGFb3
Huang Y, Xing H, Tian J, Zhang D, Zhang J, Pichurin J, Lu J, Raredon M, Kyriakides T. TSP2 Deficiency Promotes Fibroblast Proliferation and Migration With Enhanced WNT4/β‐Catenin/TGFb3. The FASEB Journal 2025, 39: e71368. PMID: 41427771, DOI: 10.1096/fj.202501884r.Peer-Reviewed Original ResearchMeSH Keywords and ConceptsConceptsTranscriptomic consequencesRNA sequencingExtracellular matrixSignaling pathwayMurine primary fibroblastsThrombospondin-2Extracellular matrix interactionsExtracellular matrix remodelingFibroblast proliferationTissue repairFibroblast functionNIH3T3 fibroblastsTGF-b3Primary fibroblastsWnt/b-catenin signaling pathwayThrombospondin-2-deficiencyChronic woundsPrimary cellsHealing-impairedMatricellular glycoproteinTherapeutic targetHealthcare burdenWnt/b-cateninFibroblastsDermal fibroblastsLung adenocarcinoma cells respond differently to mechanical stress in 3D versus 2D environments
Kitamura N, Iwatake M, Mizoguchi S, Ibrahim Wani S, Kobayashi K, Hasnain M, Nguyen V, Yokoyama R, Kitade N, Ojima T, Shimoyama K, Koba N, Hatta H, Raredon M, Hirabayashi K, Morinaga Y, Tsuchiya T. Lung adenocarcinoma cells respond differently to mechanical stress in 3D versus 2D environments. Communications Biology 2025, 8: 1819. PMID: 41381717, PMCID: PMC12749616, DOI: 10.1038/s42003-025-09179-1.Peer-Reviewed Original ResearchAltmetricConceptsComplex mechanical cuesLung adenocarcinoma cellsNuclear translocationCell adhesion-related genesAdhesion-related genesTumor suppressor geneUpregulation of tumor-suppressor genesRespiratory motionAdenocarcinoma cellsHuman lung adenocarcinoma cellsSuppressor geneCancer researchCell adhesionUpregulation of extracellular matrixIntegrin B1E-cadherinExtracellular matrixCancer cell dynamicsCell proliferationNuclear translocation of b-cateninGenesLung cancer modelCell dynamicsCellsTissue microenvironmentAltered Epithelial-Mesenchymal Progenitor States Lead to Matrix Deposition, Tissue Inflammation, and Transitional Epithelial State in Congenital Diaphragmatic Hernia
Rivero R, Edelstein S, Haynes C, Mizoguchi S, Wang N, Saltzman M, Stitelman D, Raredon M. Altered Epithelial-Mesenchymal Progenitor States Lead to Matrix Deposition, Tissue Inflammation, and Transitional Epithelial State in Congenital Diaphragmatic Hernia. Fetal And Pediatric Pathology 2025, 44: 551-572. PMID: 41246903, PMCID: PMC13014129, DOI: 10.1080/15513815.2025.2585371.Peer-Reviewed Original ResearchMeSH Keywords and ConceptsConceptsCongenital diaphragmatic herniaEpithelial-mesenchymal transitionAlveolar type 1Lung hypoplasiaDiaphragmatic herniaMesenchymal progenitorsNormal lungEpithelial-mesenchymal transition scoresFetal rat lungFibrotic lung diseaseDistal epithelial cellsPulmonary hypertensionMesenchymal-like characteristicsEpithelial-like characteristicsTissue inflammationSingle cell RNA sequencingLung diseaseAT2 cellsSaccular stageMesenchymal characteristicsRat lungEpithelial cellsPlasticity markersExtracellular matrixInflammatory signaling
Academic Achievements & Community Involvement
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Honors
honor MD/PhD Thesis Prize
05/23/2022Yale School of Medicine AwardYale School of MedicineDetailsUnited Stateshonor Draper Fellowship
09/05/2012Other AwardDraper LaboratoriesDetailsUnited Stateshonor Distinction in Biomedical Engineering
05/05/2011Yale University AwardYale UniversityDetailsUnited Stateshonor Distinction in History of Art
05/05/2011Yale University AwardYale UniversityDetailsUnited Stateshonor Engineering Honors
05/01/2011National AwardTau Beta PiDetailsUnited States
Links
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Media
- Photo by Micha Sam Brickman Raredon
Immunostaining of cellular communities at the bronchioalveolar junction in lung tissue
Get In Touch
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Contacts
Vascular Biology and Therapeutics Program
10 Amistad Street, Rm. 301A
New Haven, Connecticut 06519
United States