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
- Cardiac Surgery
- Investigative Medicine Program
- NIH T32 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
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 homeostasisVascular endothelial cells derived from transgene-free pig induced pluripotent stem cells for vascular tissue engineering
Batty L, Park J, Qin L, Riaz M, Lin Y, Xu Z, Gao X, Li X, Lopez C, Zhang W, Hoareau M, Fallon M, Huang Y, Luo H, Luo J, Ménoret S, Li P, Jiang Z, Smith P, Sachs D, Tellides G, Anegon I, Pober J, Liu P, Qyang Y. Vascular endothelial cells derived from transgene-free pig induced pluripotent stem cells for vascular tissue engineering. Acta Biomaterialia 2024, 193: 171-184. PMID: 39681154, PMCID: PMC12212065, DOI: 10.1016/j.actbio.2024.12.033.Peer-Reviewed Original ResearchInduced pluripotent stem cellsVascular tissue engineeringPig induced pluripotent stem cellsPluripotent stem cellsEndothelial cellsLarge animal modelStem cellsAnimal modelsTissue engineeringInferior vena cava graftHuman induced pluripotent stem cellsEffective differentiation protocolsPreclinical large animal modelExpression of endothelial markersCell-based therapiesExtensive preclinical testingPig endothelial cellsFunctional endothelial cellsIn vivo functional studiesTreatment of cardiovascular diseasesVascular endothelial cellsTissue engineering therapiesTransplant therapeuticsEfficacy of tissueImmunodeficient ratsFully biologic endothelialized-tissue-engineered vascular conduits provide antithrombotic function and graft patency
Park J, Riaz M, Qin L, Zhang W, Batty L, Fooladi S, Kural M, Li X, Luo H, Xu Z, Wang J, Banno K, Gu S, Yuan Y, Anderson C, Ellis M, Zhou J, Luo J, Shi X, Shin J, Liu Y, Lee S, Yoder M, Elder R, Mak M, Thorn S, Sinusas A, Gruber P, Hwa J, Tellides G, Niklason L, Qyang Y. Fully biologic endothelialized-tissue-engineered vascular conduits provide antithrombotic function and graft patency. Cell Stem Cell 2024, 32: 137-143.e6. PMID: 39644899, PMCID: PMC11698629, DOI: 10.1016/j.stem.2024.11.006.Peer-Reviewed Original ResearchTissue-engineered vascular conduitsSingle-ventricle congenital heart defectsEndothelial cellsBiodegradable polymeric scaffoldsGraft patencyAutologous bone marrow cellsAntithrombotic functionCongenital heart defectsInferior vena cava graftHiPSC-derived endothelial cellsBone marrow cellsHuman umbilical arteryDecellularized human umbilical arteriesPolymeric scaffoldsHost endothelial cellsHuman induced pluripotent stem cell (hiPSC)-derived endothelial cellsUmbilical arteryHeart defectsVascular conduitsMarrow cellsFlow bioreactorVena cava graftNude ratsGraft stenosisClinical trialsEndothelial TGF-β Signaling Regulates Endothelial-Mesenchymal Transition During Arteriovenous Fistula Remodeling in Mice With Chronic Kidney Disease
Zhang W, Gonzalez L, Li X, Bai H, Li Z, Taniguchi R, Langford J, Ohashi Y, Thaxton C, Aoyagi Y, Yatsula B, Martin K, Goodwin J, Tellides G, Long X, Shu C, Dardik A. Endothelial TGF-β Signaling Regulates Endothelial-Mesenchymal Transition During Arteriovenous Fistula Remodeling in Mice With Chronic Kidney Disease. Arteriosclerosis Thrombosis And Vascular Biology 2024, 44: 2509-2526. PMID: 39297205, PMCID: PMC11593991, DOI: 10.1161/atvbaha.124.320933.Peer-Reviewed Original ResearchChronic kidney diseaseTGF-b signalingArteriovenous fistula patencyArteriovenous fistulaKidney diseaseAVF patencyEndothelial cellsAssociated with endothelial injuryArteriovenous fistula diameterImprove AVF patencyIncreased outward remodelingReduced patencyInduced endothelial-to-mesenchymal transitionAortocaval fistula modelSmooth muscle cell proliferationArteriovenous fistula failureAttenuated EndMTEnd-stage kidney diseaseHuman arteriovenous fistulaeSmooth muscle cellsMuscle cell proliferationEndothelial-to-mesenchymal transitionMouse endothelial cellsInhibition of EndMTEndothelial-mesenchymal transition
News
News
- 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
- July 27, 2022
Uncovering New Approaches to a Common Inherited Heart Disorder
Get In Touch
Contacts
Academic Office Number
Mailing Address
Cardiac Surgery
PO Box 208062
New Haven, CT 06520-8062
United States