Hyung Chun, MD, FAHA
Associate Professor AdjunctDownloadHi-Res Photo
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Cardiovascular Medicine
Primary
Contact Info
Cardiovascular Medicine
300 George St
New Haven, CT 06511
United States
About
Titles
Associate Professor Adjunct
Appointments
Cardiovascular Medicine
Associate Professor AdjunctPrimary
Other Departments & Organizations
- Cardiovascular Medicine
- Chun Lab
- Internal Medicine
- Molecular Medicine, Pharmacology, and Physiology
- Pathology Research
- Pulmonary Vascular Disease Program
- Yale Cardiovascular Research Center (YCVRC)
- Yale Combined Program in the Biological and Biomedical Sciences (BBS)
- Yale Ventures
Education & Training
- Visiting Scholar
- University of Cambridge (2017)
- Chief Fellow
- Stanford University (2009)
- Fellowship
- Stanford University (2009)
- Residency
- Stanford University (2004)
- MD
- Johns Hopkins University School of Medicine (2002)
- Cloisters Scholar
- HHMI (2001)
- BA
- Harvard University, Biochemical Sciences (1995)
Research
Overview
Medical Research Interests
Biological Science Disciplines; Cardiovascular Diseases; Endocrine System Diseases; Respiratory Tract Diseases
Research at a Glance
Yale Co-Authors
Frequent collaborators of Hyung Chun's published research.
Publications Timeline
A big-picture view of Hyung Chun's research output by year.
Christine Won, MD, MSc, BA
Alexander B. Pine, MD, PhD
George Goshua, MD, MSc, FACP
Hanming Zhang, PhD
Marcus Shallow
Stephanie Halene, MD, Dr Med
14Publications
2,125Citations
Publications
2022
BMPR1A promotes ID2–ZEB1 interaction to suppress excessive endothelial to mesenchymal transition
Lee H, Adachi T, Pak B, Park S, Hu X, Choi W, Kowalski PS, Chang CH, Clapham KR, Lee A, Papangeli I, Kim J, Han O, Park J, Anderson DG, Simons M, Jin S, Chun HJ. BMPR1A promotes ID2–ZEB1 interaction to suppress excessive endothelial to mesenchymal transition. Cardiovascular Research 2022, 119: 813-825. PMID: 36166408, PMCID: PMC10409893, DOI: 10.1093/cvr/cvac159.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAnimalsBone Morphogenetic Protein Receptors, Type IEndothelial CellsEndotheliumEpithelial-Mesenchymal TransitionHypertension, PulmonaryInhibitor of Differentiation Protein 2LungMicePulmonary Arterial HypertensionReceptor, Transforming Growth Factor-beta Type IIZinc Finger E-box-Binding Homeobox 1ConceptsPathogenesis of PAHPulmonary arterial hypertensionEndothelial cellsOnset of PAHAmeliorate pulmonary arterial hypertensionPotential novel therapeutic targetType 1 receptorType 2 receptorEndothelial-mesenchymal transitionNovel therapeutic targetGrowth factor-beta stimulationSmooth muscle cellsBone morphogenetic proteinPAH patientsArterial hypertensionVascular disordersBMP type 1 receptorsResponse of ECsAdult miceEndoMTTherapeutic targetBeta stimulationPathogenesisMesenchymal transitionMuscle cells
2021
Severe breakthrough COVID-19 cases in the SARS-CoV-2 delta (B.1.617.2) variant era
Wang SY, Juthani PV, Borges KA, Shallow MK, Gupta A, Price C, Won CH, Chun HJ. Severe breakthrough COVID-19 cases in the SARS-CoV-2 delta (B.1.617.2) variant era. The Lancet Microbe 2021, 3: e4-e5. PMID: 34901896, PMCID: PMC8641954, DOI: 10.1016/s2666-5247(21)00306-2.Peer-Reviewed Original ResearchCitationsAltmetricMeSH KeywordsHospitalisation among vaccine breakthrough COVID-19 infections
Juthani PV, Gupta A, Borges KA, Price CC, Lee AI, Won CH, Chun HJ. Hospitalisation among vaccine breakthrough COVID-19 infections. The Lancet Infectious Diseases 2021, 21: 1485-1486. PMID: 34506735, PMCID: PMC8423430, DOI: 10.1016/s1473-3099(21)00558-2.Peer-Reviewed Original ResearchCitationsAltmetricA neutrophil activation signature predicts critical illness and mortality in COVID-19
Meizlish ML, Pine AB, Bishai JD, Goshua G, Nadelmann ER, Simonov M, Chang CH, Zhang H, Shallow M, Bahel P, Owusu K, Yamamoto Y, Arora T, Atri DS, Patel A, Gbyli R, Kwan J, Won CH, Dela Cruz C, Price C, Koff J, King BA, Rinder HM, Wilson FP, Hwa J, Halene S, Damsky W, van Dijk D, Lee AI, Chun HJ. A neutrophil activation signature predicts critical illness and mortality in COVID-19. Blood Advances 2021, 5: 1164-1177. PMID: 33635335, PMCID: PMC7908851, DOI: 10.1182/bloodadvances.2020003568.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsCritical illnessHealth system databaseNeutrophil activationCOVID-19Neutrophil activation signatureSevere COVID-19Intensive care unitGranulocyte colony-stimulating factorHigh mortality rateColony-stimulating factorSystem databaseHepatocyte growth factorClinical decompensationNeutrophil countImmune hyperactivationCare unitEarly elevationLipocalin-2Interleukin-8Longitudinal cohortClinical dataMortality ratePatientsIllnessActivation signature
2020
Endotheliopathy in COVID-19-associated coagulopathy: evidence from a single-centre, cross-sectional study
Goshua G, Pine AB, Meizlish ML, Chang CH, Zhang H, Bahel P, Baluha A, Bar N, Bona RD, Burns AJ, Dela Cruz CS, Dumont A, Halene S, Hwa J, Koff J, Menninger H, Neparidze N, Price C, Siner JM, Tormey C, Rinder HM, Chun HJ, Lee AI. Endotheliopathy in COVID-19-associated coagulopathy: evidence from a single-centre, cross-sectional study. The Lancet Haematology 2020, 7: e575-e582. PMID: 32619411, PMCID: PMC7326446, DOI: 10.1016/s2352-3026(20)30216-7.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAdultAgedAged, 80 and overBetacoronavirusBiomarkersBlood Coagulation DisordersCoronavirus InfectionsCOVID-19Critical IllnessCross-Sectional StudiesEndothelium, VascularFemaleFollow-Up StudiesHumansIntensive Care UnitsMaleMiddle AgedPandemicsPneumonia, ViralPrognosisSARS-CoV-2Vascular DiseasesYoung AdultConceptsCOVID-19-associated coagulopathyNon-ICU patientsIntensive care unitKaplan-Meier analysisSoluble P-selectinCross-sectional studyPlatelet activationHospital dischargeICU patientsSoluble thrombomodulinEndothelial cellsVWF antigenCOVID-19P-selectinSingle-center cross-sectional studyLaboratory-confirmed COVID-19Medical intensive care unitSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pathogenesisVon Willebrand factor antigenSoluble thrombomodulin concentrationsVWF antigen concentrationEndothelial cell injurySoluble CD40 ligandMicrovascular complicationsAdult patients
2017
Endothelial APLNR regulates tissue fatty acid uptake and is essential for apelin’s glucose-lowering effects
Hwangbo C, Wu J, Papangeli I, Adachi T, Sharma B, Park S, Zhao L, Ju H, Go GW, Cui G, Inayathullah M, Job JK, Rajadas J, Kwei SL, Li MO, Morrison AR, Quertermous T, Mani A, Red-Horse K, Chun HJ. Endothelial APLNR regulates tissue fatty acid uptake and is essential for apelin’s glucose-lowering effects. Science Translational Medicine 2017, 9 PMID: 28904225, PMCID: PMC5703224, DOI: 10.1126/scitranslmed.aad4000.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsGlucose-lowering effectImpaired glucose utilizationForkhead box protein O1Glucose utilizationType 2 diabetes mellitusEndothelial cellsApelin/APLNRSkeletal muscleTissue fatty acid uptakeType 2 diabetesImportant clinical challengeFatty acid uptakeEndothelial-specific deletionBox protein O1FABP4 inhibitionCardiovascular outcomesPeptide apelinDiabetes mellitusGlucose loweringFatty acidsInsulin sensitivityEndothelial expressionClinical challengeFABP4 expressionMetabolic disorders
2016
MicroRNA 139-5p coordinates APLNR-CXCR4 crosstalk during vascular maturation
Papangeli I, Kim J, Maier I, Park S, Lee A, Kang Y, Tanaka K, Khan OF, Ju H, Kojima Y, Red-Horse K, Anderson DG, Siekmann AF, Chun HJ. MicroRNA 139-5p coordinates APLNR-CXCR4 crosstalk during vascular maturation. Nature Communications 2016, 7: 11268. PMID: 27068353, PMCID: PMC4832062, DOI: 10.1038/ncomms11268.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsRetinal vascular defectsMiR-139-5pG protein-coupled receptorsVascular defectsGPCR crosstalkProtein-coupled receptorsVascular developmentCXCR4 expressionCXCR4 axisCXCR4 signalingDownstream signaling cascadesVascular phenotypePharmacological inhibitionVascular maturationDeficient stateApelinAPLNRLigand-receptor pairsSignaling cascadesInhibitionCXCR4MiceReceptors
2014
Restoration of Impaired Endothelial Myocyte Enhancer Factor 2 Function Rescues Pulmonary Arterial Hypertension
Kim J, Hwangbo C, Hu X, Kang Y, Papangeli I, Mehrotra D, Park H, Ju H, McLean DL, Comhair SA, Erzurum SC, Chun HJ. Restoration of Impaired Endothelial Myocyte Enhancer Factor 2 Function Rescues Pulmonary Arterial Hypertension. Circulation 2014, 131: 190-199. PMID: 25336633, PMCID: PMC4293354, DOI: 10.1161/circulationaha.114.013339.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAnimalsApelinArteriolesCells, CulturedDisease Models, AnimalDrug Evaluation, PreclinicalEndothelial CellsFibroblast Growth Factor 2HemodynamicsHistone Deacetylase InhibitorsHydroxamic AcidsHypertension, PulmonaryHypertrophy, Right VentricularHypoxiaIntercellular Signaling Peptides and ProteinsMaleMEF2 Transcription FactorsMicroRNAsMonocrotalinePulmonary ArteryPyrrolesRatsRats, Sprague-DawleyRNA InterferenceRNA, Small InterferingTranscription, GeneticConceptsPulmonary arterial hypertensionPulmonary artery endothelial cellsPulmonary vascular homeostasisPAH-pulmonary artery endothelial cellsMyocyte enhancer factor 2Arterial hypertensionCauses of PAHVascular homeostasisExperimental pulmonary hypertension modelsIncreased pulmonary arterial pressurePulmonary artery smooth muscle cellsArtery smooth muscle cellsMEF2 activityRight ventricular failurePulmonary arterial pressurePulmonary hypertension modelPotential therapeutic strategyPotential therapeutic valueSmooth muscle cellsArtery endothelial cellsFactor 2Potential adverse effectsTranscription factor myocyte enhancer factor 2Class IIa HDACsVentricular failure
2013
Apelin-APJ Signaling Is a Critical Regulator of Endothelial MEF2 Activation in Cardiovascular Development
Kang Y, Kim J, Anderson JP, Wu J, Gleim SR, Kundu RK, McLean DL, Kim JD, Park H, Jin SW, Hwa J, Quertermous T, Chun HJ. Apelin-APJ Signaling Is a Critical Regulator of Endothelial MEF2 Activation in Cardiovascular Development. Circulation Research 2013, 113: 22-31. PMID: 23603510, PMCID: PMC3739451, DOI: 10.1161/circresaha.113.301324.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsActive Transport, Cell NucleusAdipokinesAnimalsApelinApelin ReceptorsCardiovascular AbnormalitiesCardiovascular SystemEndocardiumEndothelium, VascularFemaleFetal HeartGene Expression Regulation, DevelopmentalGenes, LethalGTP-Binding Protein alpha Subunits, G12-G13Histone DeacetylasesIntercellular Signaling Peptides and ProteinsKruppel-Like Transcription FactorsMaleMEF2 Transcription FactorsMiceMice, Inbred C57BLMice, KnockoutMyogenic Regulatory FactorsPhosphorylationProtein Processing, Post-TranslationalReceptors, G-Protein-CoupledSignal TransductionTranscription, GeneticConceptsCardiovascular developmentVentricular wall developmentMyocyte enhancer factor 2Embryonic lethal phenotypeCardiovascular developmental defectsFactor 2Apelin-APJHistone deacetylase 4MEF2 functionModel organismsLethal phenotypeEmbryonic lethalityTranscriptional targetsMEF2 activationKrüppel-like factor 2Wall developmentHDAC5 phosphorylationCushion formationNuclear localizationVascular smooth muscle cellsEndothelial cellsDevelopmental defectsMolecular mechanismsCritical regulatorLigand apelin
2012
An endothelial apelin-FGF link mediated by miR-424 and miR-503 is disrupted in pulmonary arterial hypertension
Kim J, Kang Y, Kojima Y, Lighthouse JK, Hu X, Aldred MA, McLean DL, Park H, Comhair SA, Greif DM, Erzurum SC, Chun HJ. An endothelial apelin-FGF link mediated by miR-424 and miR-503 is disrupted in pulmonary arterial hypertension. Nature Medicine 2012, 19: 74-82. PMID: 23263626, PMCID: PMC3540168, DOI: 10.1038/nm.3040.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAnimalsApelinCell MovementCell ProliferationCells, CulturedCulture Media, ConditionedDown-RegulationEndothelial CellsFamilial Primary Pulmonary HypertensionFibroblast Growth Factor 2HumansHypertension, PulmonaryIntercellular Signaling Peptides and ProteinsMiceMice, Inbred C57BLMice, KnockoutMicroRNAsMuscle, Smooth, VascularMyocytes, Smooth MusclePulmonary ArteryRatsReceptor, Fibroblast Growth Factor, Type 1RNA InterferenceRNA, Small InterferingSignal TransductionVascular DiseasesConceptsPulmonary arterial hypertensionArterial hypertensionVascular smooth muscle cellsPulmonary endothelial cellsSmooth muscle cellsEndothelial cell proliferationPulmonary hypertensionPeptide apelinCytokine productionRat modelVascular homeostasisHypertensionMiR-503MiR-424Endothelial cellsCell proliferation
Academic Achievements & Community Involvement
activity American Society for Clinical Investigation
Professional OrganizationsMemberDetails04/01/2016 - Presentactivity Fellow of the American Heart Association
Professional OrganizationsMemberDetails11/13/2015 - Present
News
News
- April 27, 2023
Study Uncovers Reduced Exercise Tolerance and Other Changes in Long COVID
- October 28, 2022Source: TCTMD
COVID Vaccine Thrombosis, Thrombocytopenia Risks Clarified in International Study
- June 15, 2022
Best wishes to Dr. Hyung Chun
- May 16, 2022
Elevated Biomarkers Offer Early Indicator of Severe COVID-19, Study Says
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Cardiovascular Medicine
300 George St
New Haven, CT 06511
United States