Hanqiang Deng, PhD
Associate Research Scientist (Cardiovascular Medicine)DownloadHi-Res Photo
Cards
Appointments
Cardiovascular Medicine
Primary
Contact Info
Cardiovascular Medicine
300 George Street, Room 759
New Haven, CT 06511
United States
About
Titles
Associate Research Scientist (Cardiovascular Medicine)
Appointments
Cardiovascular Medicine
Associate Research ScientistPrimary
Other Departments & Organizations
- Cardiovascular Medicine
- Internal Medicine
- Schwartz Lab
Education & Training
- Postdoctoral Researcher
- Yale University School of Medicine, Yale Cardiovascular Research Center (2022)
- PhD
- Shanghai Jiao Tong University, School of Medicine (2016)
Research
Overview
Medical Research Interests
Atherosclerosis; Cardiovascular Diseases; Inflammation; Pulmonary Arterial Hypertension
ORCID
0000-0001-5976-517X- View Lab Website
Schwartz Lab
Research at a Glance
Yale Co-Authors
Frequent collaborators of Hanqiang Deng's published research.
Publications Timeline
A big-picture view of Hanqiang Deng's research output by year.
Research Interests
Research topics Hanqiang Deng is interested in exploring.
Martin Schwartz, PhD
Angeliki Louvi, PhD
Carlos Fernandez-Hernando, PhD
Jiasheng Zhang, MD
Minghao Chen, MD/PhD
8Publications
163Citations
Atherosclerosis
Publications
Featured Publications
A KLF2-BMPER-Smad1/5 checkpoint regulates high fluid shear stress-mediated artery remodeling
Deng H, Zhang J, Wang Y, Joshi D, Pi X, De Val S, Schwartz M. A KLF2-BMPER-Smad1/5 checkpoint regulates high fluid shear stress-mediated artery remodeling. Nature Cardiovascular Research 2024, 3: 785-798. PMID: 39196179, DOI: 10.1038/s44161-024-00496-y.Peer-Reviewed Original ResearchCitationsAltmetricConceptsFluid shear stressVascular remodelingOutward remodelingBone morphogenetic proteinShear stressMouse models of type 1Ischemic diseasesModels of type 1BMP-binding endothelial regulatorBlood flow recoveryType 2 diabetesPhysiological fluid shear stressPotential therapeutic approachBlocking antibodiesMouse modelSmad1/5 activationArterial remodelingTherapeutic approachesType 1Akt activationBlood flowEndothelial regulationSmad1/5Flow recoveryMorphogenetic proteins
2024
Endothelial γ-protocadherins inhibit KLF2 and KLF4 to promote atherosclerosis
Joshi D, Coon B, Chakraborty R, Deng H, Yang Z, Babar M, Fernandez-Tussy P, Meredith E, Attanasio J, Joshi N, Traylor J, Orr A, Fernandez-Hernando C, Libreros S, Schwartz M. Endothelial γ-protocadherins inhibit KLF2 and KLF4 to promote atherosclerosis. Nature Cardiovascular Research 2024, 3: 1035-1048. PMID: 39232138, PMCID: PMC11399086, DOI: 10.1038/s44161-024-00522-z.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAnimalsAtherosclerosisCadherin Related ProteinsCadherinsDisease Models, AnimalEndothelial CellsHuman Umbilical Vein Endothelial CellsHumansKruppel-Like Factor 4Kruppel-Like Transcription FactorsMaleMiceMice, Inbred C57BLMice, KnockoutPlaque, AtheroscleroticReceptors, NotchSignal TransductionConceptsAtherosclerotic cardiovascular diseaseIntracellular domainNotch intracellular domainTranscription factor KLF2Mechanisms of vascular inflammationAnti-inflammatory programVascular endothelial cellsHost defenseCleavage resultsAntibody blockadeGenetic deletionVascular inflammationViral infectionImmune systemEndothelial cellsCardiovascular diseasePromote atherosclerosisBlood flowKLF2KLF4Suppressive signalsEndotheliumMechanistic studies
2022
Endothelial mechanosensing: A forgotten target to treat vascular remodeling in hypertension?
Tiezzi M, Deng H, Baeyens N. Endothelial mechanosensing: A forgotten target to treat vascular remodeling in hypertension? Biochemical Pharmacology 2022, 206: 115290. PMID: 36241094, DOI: 10.1016/j.bcp.2022.115290.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsFuture drug development strategiesMechanistic cuesVascular remodelingNew potential therapeutic approachReceptor complexIon channelsPulmonary arterial hypertensionMechanosensitive organMesenchymal transitionPotential therapeutic approachDrug development strategiesCommon mechanismPleiotropic actionsArterial hypertensionEssential hypertensionEndothelial inflammationTherapeutic approachesBlood flowTissue perfusionVascular integrityHypertensionDistinct diseasesCrucial roleRecent studiesRemodelingHigh Fluid Shear Stress Inhibits Cytokine‐Driven Smad2/3 Activation in Vascular Endothelial Cells
Deng H, Schwartz MA. High Fluid Shear Stress Inhibits Cytokine‐Driven Smad2/3 Activation in Vascular Endothelial Cells. Journal Of The American Heart Association 2022, 11: e025337. PMID: 35861829, PMCID: PMC9707828, DOI: 10.1161/jaha.121.025337.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsInflammatory cytokinesSmad2/3 activationEndothelial cellsNuclear translocationInflammatory cytokine treatmentGrowth factor betaVascular endothelial cellsQuantitative polymerase chain reactionSmad2/3 nuclear translocationTarget gene expressionBackground AtherosclerosisInflammatory mediatorsInflammatory pathwaysPolymerase chain reactionResult of inhibitionCytokine treatmentInhibits CytokineFactor betaMesenchymal transitionHigh fluid shear stressCytokinesEndMTGene expressionLaminar fluid shear stressFluid shear stress
2021
MEKK3–TGFβ crosstalk regulates inward arterial remodeling
Deng H, Xu Y, Hu X, Zhuang ZW, Chang Y, Wang Y, Ntokou A, Schwartz MA, Su B, Simons M. MEKK3–TGFβ crosstalk regulates inward arterial remodeling. Proceedings Of The National Academy Of Sciences Of The United States Of America 2021, 118: e2112625118. PMID: 34911761, PMCID: PMC8713777, DOI: 10.1073/pnas.2112625118.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAnimalsGene DeletionGene Expression RegulationGenotypeHindlimbHuman Umbilical Vein Endothelial CellsHumansHypertension, PulmonaryIschemiaMAP Kinase Kinase Kinase 1MAP Kinase Kinase Kinase 3MiceReceptors, Transforming Growth Factor betaSelective Estrogen Receptor ModulatorsSignal TransductionTamoxifenTransforming Growth Factor betaVascular RemodelingConceptsArterial remodelingSuch common diseasesEndothelial-specific deletionActivation of TGFβArtery diseaseHyperlipidemic miceSpontaneous hypertensionInward remodelingAccelerated progressionArterial diameterVascular remodelingPathogenic importanceAdult miceKnockout miceVascular circuitPathologic conditionsCommon diseaseMAPK ERK1/2MiceRemodelingHypertensionAtherosclerosisControl of proliferationDiseaseProgressionActivation of Smad2/3 signaling by low fluid shear stress mediates artery inward remodeling
Deng H, Min E, Baeyens N, Coon BG, Hu R, Zhuang ZW, Chen M, Huang B, Afolabi T, Zarkada G, Acheampong A, McEntee K, Eichmann A, Liu F, Su B, Simons M, Schwartz MA. Activation of Smad2/3 signaling by low fluid shear stress mediates artery inward remodeling. Proceedings Of The National Academy Of Sciences Of The United States Of America 2021, 118: e2105339118. PMID: 34504019, PMCID: PMC8449390, DOI: 10.1073/pnas.2105339118.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsLow fluid shear stressFluid shear stressNuclear translocationSmad linker regionTransmembrane protein Neuropilin-1Target gene expressionCyclin-dependent kinasesBone morphogenetic proteinEC-specific deletionSmad2/3 nuclear translocationNuclear localizationHigh fluid shear stressLinker regionMorphogenetic proteinsGene expressionRegulatory mechanismsActivation of Smad2/3Receptor ALK5Smad2/3 phosphorylationTranslocationCell sensingEndothelial cell (EC) sensingPhosphorylationALK5Smad2/3
2015
Structure and vascular function of MEKK3–cerebral cavernous malformations 2 complex
Fisher OS, Deng H, Liu D, Zhang Y, Wei R, Deng Y, Zhang F, Louvi A, Turk BE, Boggon TJ, Su B. Structure and vascular function of MEKK3–cerebral cavernous malformations 2 complex. Nature Communications 2015, 6: 7937. PMID: 26235885, PMCID: PMC4526114, DOI: 10.1038/ncomms8937.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAnimalsAnimals, NewbornBlood VesselsCapillary PermeabilityCerebrovascular CirculationCrystallizationHemangioma, Cavernous, Central Nervous SystemIntracranial HemorrhagesMAP Kinase Kinase Kinase 3MiceMice, KnockoutMicrofilament ProteinsNeovascularization, PhysiologicRho GTP-Binding ProteinsRho-Associated KinasesSignal Transduction
2014
The DNA methylation-regulated miR-193a-3p dictates the multi-chemoresistance of bladder cancer via repression of SRSF2/PLAU/HIC2 expression.
Lv L, Deng H, Li Y, Zhang C, Liu X, Liu Q, Zhang D, Wang L, Pu Y, Zhang H, He Y, Wang Y, Yu Y, Yu T, Zhu J. The DNA methylation-regulated miR-193a-3p dictates the multi-chemoresistance of bladder cancer via repression of SRSF2/PLAU/HIC2 expression. Cell Death & Disease 2014, 5: e1402. PMID: 25188512, PMCID: PMC4540198, DOI: 10.1038/cddis.2014.367.Peer-Reviewed Original Research
Academic Achievements & Community Involvement
activity American Heart Association
Professional OrganizationsMemberDetails11/12/2021 - Presentactivity North American Vascular Biology Organization
Professional OrganizationsMemberDetails11/11/2021 - Presentactivity North American Vascular Biology Organization
Professional OrganizationsProgram CommitteeDetails2022 - Presentactivity North American Vascular Biology Organization
CommitteesCommittee MemberDetails02/01/2022 - Presentactivity American Heart Association
Peer Review Groups and Grant Study SectionsAd-hoc reviewerDetails03/01/2024 - Present
News & Links
Media
News
Get In Touch
Contacts
Mailing Address
Cardiovascular Medicine
300 George Street, Room 759
New Haven, CT 06511
United States
Locations
300 George Street
Lab
New Haven, CT 06511