Yan Huang, PhD
Associate Research Scientist in Medicine (Comparative Medicine)DownloadHi-Res Photo
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Associate Research Scientist in Medicine (Comparative Medicine)
Appointments
Comparative Medicine
Associate Research ScientistPrimary
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Education & Training
- PhD
- Hunan Medical University (1998)
Research
Research at a Glance
Yale Co-Authors
Frequent collaborators of Yan Huang's published research.
Publications Timeline
A big-picture view of Yan Huang's research output by year.
Muhammad Riaz, PhD, MPhil
Yibing Qyang, PhD
Stuart Campbell
Christopher Anderson, BSc
Diane Krause, MD, PhD
George Tellides, MD, PhD
28Publications
3,585Citations
Publications
2024
De Novo Elastin Assembly Alleviates Development of Supravalvular Aortic Stenosis—Brief Report
Ellis M, Riaz M, Huang Y, Anderson C, Hoareau M, Li X, Luo H, Lee S, Park J, Luo J, Batty L, Huang Q, Lopez C, Reinhardt D, Tellides G, Qyang Y. De Novo Elastin Assembly Alleviates Development of Supravalvular Aortic Stenosis—Brief Report. Arteriosclerosis Thrombosis And Vascular Biology 2024, 44: 1674-1682. PMID: 38752350, PMCID: PMC11209776, DOI: 10.1161/atvbaha.124.320790.Peer-Reviewed Original ResearchAltmetricConceptsSupravalvular aortic stenosisVascular smooth muscle cellsSmooth muscle cellsMuscle cellsAortic stenosisMedial vascular smooth muscle cellsVascular proliferative diseasesEpigallocatechin gallate treatmentProliferative abnormalitiesPreclinical findingsHeart failureLuminal occlusionMouse modelCell hyperproliferationDefective elastinProliferative diseasesCardiovascular disordersFormation of elastinTherapeutic interventionsElastin assemblyElastin depositionStenosisMiceAortic mechanicsImproper formation
2019
Tissue-Engineered Stem Cell Models of Cardiovascular Diseases
Anderson C, Luo J, Sewanan L, Kural M, Riaz M, Park J, Huang Y, Niklason L, Campbell S, Qyang Y. Tissue-Engineered Stem Cell Models of Cardiovascular Diseases. 2019, 1-18. DOI: 10.1007/978-3-030-20047-3_1.ChaptersAltmetricConceptsMolecular underpinningsStem cell modelTwo-dimensional cell culture methodsComplex 3D microenvironmentThree-dimensional microenvironmentMolecular mechanismsTissue-engineered modelDisease modelingNew therapeutic strategiesCell culturesCell culture methodsCell modelPathological conditionsCulture systemDisease statesCompelling insightsTherapeutic strategiesMicroenvironmentCulture methodVivoUse of Human Cells and Heart Muscle Tissue Patches as Therapeutics for Heart Diseases
Batty L, Ellis M, Anderson C, Luo J, Riaz M, Park J, Das S, Huang Y, Jacoby D, Campbell S, Qyang Y. Use of Human Cells and Heart Muscle Tissue Patches as Therapeutics for Heart Diseases. 2019 DOI: 10.1016/b978-0-12-801238-3.65542-3.ChaptersConceptsCardiac tissue engineeringThree-dimensional tissuesCardiovascular disease epidemicRegenerative medicineTissue engineeringCardiac patchesCardiovascular healthHeart diseaseInfarcted tissueClinical useHydrogel matrixStem cellsCardiomyocytesTissue patchesRecent innovationsDisease epidemicsTissueFurther researchHuman cells
2016
Endothelial Nogo-B regulates sphingolipid biosynthesis to promote the transition from hypertrophy to heart failure during chronic pressure overload
Zhang Y, Huang Y, Cantalupo A, Azevedo P, Siragusa M, Giordano F, Di Lorenzo A. Endothelial Nogo-B regulates sphingolipid biosynthesis to promote the transition from hypertrophy to heart failure during chronic pressure overload. International Journal Of Cardiology Cardiovascular Risk And Prevention 2016, 10: e2. DOI: 10.1016/j.jash.2016.03.006.Peer-Reviewed Original ResearchCitations
2013
Activation of Hypoxia‐Inducible Factor‐2 in Adipocytes Results in Pathological Cardiac Hypertrophy
Lin Q, Huang Y, Booth CJ, Haase VH, Johnson RS, Simon M, Giordano FJ, Yun Z. Activation of Hypoxia‐Inducible Factor‐2 in Adipocytes Results in Pathological Cardiac Hypertrophy. Journal Of The American Heart Association 2013, 2: e000548. PMID: 24326162, PMCID: PMC3886757, DOI: 10.1161/jaha.113.000548.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsMeSH KeywordsAdipocytesAnimalsBasic Helix-Loop-Helix Transcription FactorsCardiomegalyCytokinesDisease Models, AnimalGene Expression RegulationGenetic Predisposition to DiseaseHypoxia-Inducible Factor 1, alpha SubunitInflammation MediatorsMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMyocytes, CardiacPhenotypeSignal TransductionTime FactorsVon Hippel-Lindau Tumor Suppressor ProteinConceptsPathological cardiac hypertrophyCardiac hypertrophyHypoxia-inducible factor-2Hypoxia-signaling pathwayHypoxia-inducible factor (HIF) pathwayVon Hippel-Lindau (VHL) geneTranscription factorsUncharacterized mechanismAdipose tissueAdipocytes resultsHIF activationObesity-associated cardiomyopathyChemotactic protein-1Protein 1Activated T cellsDirect roleEssential roleCardiomyopathy-associated genesFactor 2Genetic deletionFactor pathwayUndefined mechanismDeletionNuclear factorGenes
2012
IL-13 receptor α2-arginase 2 pathway mediates IL-13-induced pulmonary hypertension
Cho WK, Lee CM, Kang MJ, Huang Y, Giordano FJ, Lee PJ, Trow TK, Homer RJ, Sessa WC, Elias JA, Lee CG. IL-13 receptor α2-arginase 2 pathway mediates IL-13-induced pulmonary hypertension. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2012, 304: l112-l124. PMID: 23125252, PMCID: PMC3543640, DOI: 10.1152/ajplung.00101.2012.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsConceptsPulmonary hypertensionIL-13Human pulmonary artery smooth muscle cellsDevelopment of PHPulmonary artery smooth muscle cellsRight ventricle systolic pressurePathogenesis of PHArtery smooth muscle cellsExpression of ARG2Pulmonary arterial hypertensionPulmonary vascular remodelingVentricle systolic pressurePotential therapeutic targetIL-13 treatmentSmooth muscle cellsNull mutant miceArterial hypertensionEffector cytokinesMedial thickeningSystolic pressureHemodynamic changesPulmonary arterySmall-interfering RNAVascular remodelingArginase-2Engineered Zinc-Finger Proteins Can Compensate Genetic Haploinsufficiency by Transcriptional Activation of the Wild-Type Allele: Application to Willams-Beuren Syndrome and Supravalvular Aortic Stenosis
Zhang P, Huang A, Morales-Ruiz M, Starcher BC, Huang Y, Sessa WC, Niklason LE, Giordano FJ. Engineered Zinc-Finger Proteins Can Compensate Genetic Haploinsufficiency by Transcriptional Activation of the Wild-Type Allele: Application to Willams-Beuren Syndrome and Supravalvular Aortic Stenosis. Human Gene Therapy 2012, 23: 1186-1199. PMID: 22891920, PMCID: PMC3498887, DOI: 10.1089/hum.2011.201.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAllelesAortic Stenosis, SupravalvularCell LineCell MovementCell ProliferationDosage Compensation, GeneticElastinGene ExpressionGene Expression RegulationHaploinsufficiencyHumansMutationNonsense Mediated mRNA DecayOrgan SpecificityProtein EngineeringTranscriptional ActivationWilliams SyndromeZinc FingersConceptsZinc finger protein transcription factorsTranscriptional activationWild-type alleleWilliams-Beuren syndromeMutant allelesEngineered Zinc Finger ProteinsElastin geneTargeted transcriptional activationCompensatory expressionSplice variantsZinc finger proteinProtein transcription factorsNonsense-mediated decayWild-type cellsMultiple splice variantsElastin expressionGene replacement strategyMutant proteinsHaploinsufficient genesTranscription factorsComplex genesNatural stoichiometryDistinct genetic syndromesGenesGenetic diseasesA Designed Zinc-finger Transcriptional Repressor of Phospholamban Improves Function of the Failing Heart
Zhang HS, Liu D, Huang Y, Schmidt S, Hickey R, Guschin D, Su H, Jovin IS, Kunis M, Hinkley S, Liang Y, Hinh L, Spratt SK, Case CC, Rebar EJ, Ehrlich BE, Ehrlich B, Gregory P, Giordano F. A Designed Zinc-finger Transcriptional Repressor of Phospholamban Improves Function of the Failing Heart. Molecular Therapy 2012, 20: 1508-1515. PMID: 22828502, PMCID: PMC3412484, DOI: 10.1038/mt.2012.80.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsHeart failureZinc finger protein transcription factorsSingle gene regulationZinc finger transcriptional repressorDiverse DNA sequencesProtein transcription factorsDisease-related genesDisease-related proteinsGene repressionZFP TFsTranscriptional repressorTranscription factorsDNA sequencesPotent repressionPLN expressionHuman diseasesRepressorContractile functionDrug targetsFailing HeartTherapeutic inhibitionAnimal modelsReuptake kineticsRepressionTherapeutic interventionsmiR-1 mediated suppression of Sorcin regulates myocardial contractility through modulation of Ca2+ signaling
Ali R, Huang Y, Maher SE, Kim RW, Giordano FJ, Tellides G, Geirsson A. miR-1 mediated suppression of Sorcin regulates myocardial contractility through modulation of Ca2+ signaling. Journal Of Molecular And Cellular Cardiology 2012, 52: 1027-1037. PMID: 22326846, DOI: 10.1016/j.yjmcc.2012.01.020.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsMeSH KeywordsAnimalsBase SequenceCalcium SignalingCalcium-Binding ProteinsCardiac VolumeCardiomyopathiesCell LineDEAD-box RNA HelicasesHeartHumansMaleMiceMice, 129 StrainMice, Inbred C57BLMice, KnockoutMicroRNAsMyocardial ContractionMyocardiumRibonuclease IIIRNA InterferenceRNA, Small InterferingUp-RegulationConceptsCardiac functionMiR-1Normal cardiac contractile functionEnd-stage cardiomyopathyCardiac contractile functionWild-type miceCalcium signalingExcitation-contraction couplingModulation of Ca2Cultured mouse cardiomyocytesAcute cardiomyopathyMiR-1 targetsHeart failureMyocardial contractilityMiR-1 knockdownContractile functionAntagomir treatmentSorcin expressionCalcium homeostasisKnockdown miceSorcin levelsCardiac phenotypeMouse cardiomyocytesCritical mediatorPathological relevance
2010
Cellular Endocytosis and Gene Delivery
Ziello J, Huang Y, Jovin I. Cellular Endocytosis and Gene Delivery. Molecular Medicine 2010, 16: 222-229. PMID: 20454523, PMCID: PMC2864810, DOI: 10.2119/molmed.2009.00101.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsGene therapyNonviral vectorsClathrin-independent endocytic processVariety of vectorsUnderstanding of endocytosisClathrin-dependent endocytosisCurrent molecular medicineMechanism of endocytosisGene deliveryLipid raftsEndocytic processVector deliveryCellular traffickingCellular endocytosisEndocytosisMolecular medicineTraffickingTarget cellsCellsMetabolic diseasesTherapeutic potentialCaveolaeGenesDeliveryAdeno
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