George Tellides, MD, PhD
Professor of Surgery (Cardiac)Cards
About
Titles
Professor of Surgery (Cardiac)
Biography
George Tellides, MD, PhD, earned his medical degree from the University of Witwatersrand, Johannesburg, and his PhD from the University of Oxford. Dr. Tellidies is dedicated to saving and improving the lives of patients with cardiac disease and heart failure and concentrates his clinical practice at the Veterans Affairs Medical Center, West Haven, CT.
Last Updated on April 07, 2025.
Appointments
Cardiac Surgery
ProfessorPrimary
Other Departments & Organizations
- All Institutions
- Cardiac Surgery
- Investigative Medicine Program
- Nuclear & Stress Testing
- Surgery
- Vascular Biology and Therapeutics Program
- Yale Ventures
Education & Training
- Chief Resident
- Harvard Medical School, Brigham and Women's Hospital, Boston, MA (1995)
- Resident
- Brigham and Women's Hospital and Children'sHospital, Harvard Medical School, Boston, MA (1994)
- Chief Resident
- Yale School of Medicine, Yale-New Haven Hospital, New Haven, CT (1993)
- Resident
- Yale School of Medicine, Yale-New Haven Hospital, New Haven, CT (1992)
- PhD
- University of Oxford (1988)
- Research Fellow
- John Radcliffe Hospital, University of Oxford, Oxford, England (1988)
- MD
- University of Witwatersrand (1983)
- Intern
- Johannesburg Hospital, University of the Witwatersrand Medical School, Johannesburg, South Africa
Board Certifications
Thoracic Surgery
- Certification Organization
- AB of Thoracic Surgery
- Original Certification Date
- 1996
Surgery
- Certification Organization
- AB of Surgery
- Original Certification Date
- 1994
Research
Publications
2026
FOXO1 Integrates Endothelial Hemodynamic, Inflammatory, and Metabolic Pathways in Atherosclerosis
Deng H, Zhang X, Wang Y, Joshi D, Tellides G, Schwartz M. FOXO1 Integrates Endothelial Hemodynamic, Inflammatory, and Metabolic Pathways in Atherosclerosis. Circulation Research 2026, 138: e327592. PMID: 41738126, PMCID: PMC12989233, DOI: 10.1161/circresaha.125.327592.Peer-Reviewed Original ResearchConceptsFOXO1 nuclear translocationPhysiological fluid shear stressNuclear translocationEndothelial cellsEndothelial inflammationGene expressionAdeno-associated virusTreated with cytokinesAtherosclerotic cardiovascular diseaseInflammatory gene expressionInhibition of glycolysisAssociated with glycolysisDeletion of FoxO1FOXO1 localizationHigh-cholesterol/high-fat dietPatterns in vitroPosttranslational modificationsFluid shear stressFoxo1 knockoutInflammatory cytokinesAnti-inflammatory programFOXO1 nuclear localizationNuclear localizationTranscription factorsHyperlipidemic miceProximal 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 ResearchConceptsProximal 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 signalingMiceMacrophagesSphingosine kinase 1 is integral for elastin deficiency-induced arterial hypermuscularization
Saito J, Dave J, Gallardo-Vara E, Sadagopan N, Kabir I, Tellides G, Riemer R, Urban Z, Spiegel S, Hla T, Greif D. Sphingosine kinase 1 is integral for elastin deficiency-induced arterial hypermuscularization. Nature Cardiovascular Research 2026, 5: 34-50. PMID: 41492020, DOI: 10.1038/s44161-025-00762-7.Peer-Reviewed Original ResearchConceptsSmooth muscle cellsSphingosine kinase 1Ductus arteriosusPharmacological inhibitionAortic smooth muscle cellsCongenital heart diseaseWild-type miceTranscription factor early growth response 1SMC proliferationSphingosine kinase 1 inhibitorInhibition of sphingosine kinase 1Early growth response 1Kinase 1DA patencyGrowth response 1Aortic diseaseArtery diseaseEmbryonic dayMuscle cellsTherapeutic strategiesHeart diseaseAorta of humansElastic fibersDiseaseResponse 1
2025
Role of GCC2 in T Cell Mediated Allograft Rejection in Mice
Tanvir E, Pell J, Reghuvaran A, Kumar A, Qin L, Mandel-Brahm C, Tellides G, Menon M. Role of GCC2 in T Cell Mediated Allograft Rejection in Mice. American Journal Of Transplantation 2025, 25: s875-s876. DOI: 10.1016/j.ajt.2025.07.2079.Peer-Reviewed Original ResearchIntracellular Membrane Attack Complexes Disrupt Proteostasis and Acquire Alarmin-Like Properties during Antibody-Mediated Rejection
Ma Z, He L, Mak M, Moeckel G, Tellides G, Jane-Wit D. Intracellular Membrane Attack Complexes Disrupt Proteostasis and Acquire Alarmin-Like Properties during Antibody-Mediated Rejection. American Journal Of Transplantation 2025, 25: s93. DOI: 10.1016/j.ajt.2025.07.193.Peer-Reviewed Original ResearchIntegrin-mediated mTOR signaling drives TGF-β overactivity and myxomatous mitral valve degeneration in hypomorphic fibrillin-1 mice
Gao F, Chen Q, Mori M, Li S, Ferrari G, Krane M, Fan R, Tellides G, Liu Y, Geirsson A. Integrin-mediated mTOR signaling drives TGF-β overactivity and myxomatous mitral valve degeneration in hypomorphic fibrillin-1 mice. Journal Of Clinical Investigation 2025, 135: e183558. PMID: 40392604, PMCID: PMC12259269, DOI: 10.1172/jci183558.Peer-Reviewed Original ResearchMitral valve prolapseMyxomatous mitral valve degenerationValve prolapseMitral valve degenerationValve degenerationWeeks of ageTGF-bMgR miceMitral regurgitationAssociation of mitral valve prolapseProgression of mitral valve prolapseMTOR signalingMTOR inhibitionMitral valve diseaseMTOR activityTGF-b signalingLong-term inhibitionIncreased mTOR signalingMarfan syndromeMedical therapyLeukocyte infiltrationFBN1 variantsMacrophage recruitmentValve diseaseProlapseUnderstanding 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 Human Proximal Pulmonary Artery Plays a Critical Role in Regulating Cardiopulmonary Function in Health and Disease
Manning E, Lee S, Ashadujjaman M, De Man R, Cai Z, Adams T, Raredon M, Ramachandra A, Cavinato C, Heerdt P, Singh I, Choudhary G, Yan X, Bellini C, Tellides G, Humphrey J, Kaminski N. The Human Proximal Pulmonary Artery Plays a Critical Role in Regulating Cardiopulmonary Function in Health and Disease. American Journal Of Respiratory And Critical Care Medicine 2025, 211: a2891-a2891. DOI: 10.1164/ajrccm.2025.211.abstracts.a2891.Peer-Reviewed Original ResearchShort-term disruption of TGFβ signaling in adult mice renders the aorta vulnerable to hypertension-induced dissection
Jiang B, Ren P, He C, Wang M, Murtada S, Ruiz-Rodríguez M, Chen Y, Ramachandra A, Li G, Qin L, Assi R, Schwartz M, Humphrey J, Tellides G. Short-term disruption of TGFβ signaling in adult mice renders the aorta vulnerable to hypertension-induced dissection. JCI Insight 2025, 10 PMID: 39932797, PMCID: PMC11949005, DOI: 10.1172/jci.insight.182629.Peer-Reviewed Original ResearchConceptsSmooth muscle cellsBlood pressureAortic dissectionAdult miceInherited connective tissue disorderConnective tissue disordersTGF-b signalingAccumulation of bloodHigh blood pressureAortic phenotypeTissue disordersMolecule expressionTGFB signalingMuscle cellsRisk factorsSynthesis of extracellular matrixSustained increaseTransient increaseBlood extravasationDissectionMedial injuryExtracellular matrix productionVascular degenerationExperimental modelMice
2024
Heterogeneous Cardiac-Derived and Neural Crest–Derived Aortic Smooth Muscle Cells Exhibit Similar Transcriptional Changes After TGFβ Signaling Disruption
Ren P, Jiang B, Hassab A, Li G, Li W, Assi R, Tellides G. Heterogeneous Cardiac-Derived and Neural Crest–Derived Aortic Smooth Muscle Cells Exhibit Similar Transcriptional Changes After TGFβ Signaling Disruption. Arteriosclerosis Thrombosis And Vascular Biology 2024, 45: 260-276. PMID: 39697172, PMCID: PMC12053597, DOI: 10.1161/atvbaha.124.321706.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAortaAortic AneurysmCell LineageDisease Models, AnimalGene Expression ProfilingHomeobox Protein Nkx-2.5HumansMaleMarfan SyndromeMiceMice, Inbred C57BLMice, KnockoutMuscle, Smooth, VascularMyocytes, Smooth MuscleMyosin Heavy ChainsNeural CrestPhenotypeReceptor, Transforming Growth Factor-beta Type IIReceptors, Transforming Growth Factor betaSignal TransductionSingle-Cell AnalysisTranscription, GeneticTranscriptomeTransforming Growth Factor betaWnt1 ProteinConceptsSmooth muscle cell clustersSmooth muscle cellsAortic smooth muscle cellsNeural crest-derived smooth muscle cellsCardiac derivativesMurine aortic smooth muscle cellsNeural crest originReceptor deletionAortic rootAdult miceNeural crest progenitorsNKX2-5Proximal aortaTranscriptional changesMouse modelTGFB signalingMuscle cellsConditional deletionAdult human aortaEmbryological originIncreased expressionAnalyzed single-cell transcriptomesTGFB receptorsBasal stateAortic homeostasis
Academic Achievements & Community Involvement
News
News
- January 22, 2026
Researchers Uncover Potential Pathway To Address Williams-Beuren Syndrome
- September 20, 2024
What Gets Lost When Autopsies Aren’t Done? Not Just Cause of Death
- March 11, 2024
Engineering a Heart Conduit: New $2M NIH Grant for Yale Research
- May 12, 2023
Targeting Fibronectin-integrin α5 Signaling in Marfan Syndrome
Get In Touch
Contacts
Academic Office Number
Mailing Address
Cardiac Surgery
PO Box 208062
New Haven, CT 06520-8062
United States