Hanming Zhang, PhD
Associate Research ScientistAbout
Titles
Associate Research Scientist
Education & Training
- PhD
- University of South Dakota (2019)
- BS
- Zhejiang Sci-Tech University (2012)
Research
Publications
2025
Inflamed endothelial cells express S1PR1 inhibitor CD69 to induce vascular leak
Levesque M, Cartier A, Lin Y, Sah R, Zhang H, Chaube B, Bhaumik M, Körbelin J, Suárez Y, Fernández-Hernando C, Hla T. Inflamed endothelial cells express S1PR1 inhibitor CD69 to induce vascular leak. Journal Of Biological Chemistry 2025, 301: 110455. PMID: 40617350, PMCID: PMC12336701, DOI: 10.1016/j.jbc.2025.110455.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, CDAntigens, Differentiation, T-LymphocyteCapillary PermeabilityEndothelial CellsHumansInflammationInfluenza A Virus, H1N1 SubtypeLectins, C-TypeLungMiceMice, Inbred C57BLOrthomyxoviridae InfectionsReceptors, LysosphingolipidSignal TransductionSphingosine-1-Phosphate ReceptorsConceptsAdeno-associated virus-mediated overexpressionCell surface expressionVascular leakEndothelial cellsIntranasal infectionBarrier functionMouse-adapted influenza virusTight junction protein claudin-5Viral host defenseLung vascular leakSphingosine 1-phosphate receptor 1Protein claudin-5Endothelial cell activationActivation molecule CD69Lung endothelial cellsGenetic mouse modelsEndothelial barrier functionExpression of S1PR1H1N1 infectionInfluenza virusCD69 inductionTLR3 agonistVascular leakageEndothelial activationExaggerated inflammationHypercholesterolemia-induced LXR signaling in smooth muscle cells contributes to vascular lesion remodeling and visceral function
Zhang H, de Urturi D, Fernández-Tussy P, Huang Y, Jovin D, Zhang X, Huang S, Lek M, da Silva Catarino J, Sternak M, Citrin K, Swirski F, Gustafsson J, Greif D, Esplugues E, Biwer L, Suárez Y, Fernández-Hernando C. Hypercholesterolemia-induced LXR signaling in smooth muscle cells contributes to vascular lesion remodeling and visceral function. Proceedings Of The National Academy Of Sciences Of The United States Of America 2025, 122: e2417512122. PMID: 40035761, PMCID: PMC11912459, DOI: 10.1073/pnas.2417512122.Peer-Reviewed Original ResearchConceptsVascular smooth muscle cellsSmooth muscle cellsLiver X receptorLesion remodelingMuscle cellsVascular functionArterial media layerContribution of lipid metabolismPhenotypic switchingRegulate vascular toneMonocyte-derived macrophagesLipid metabolismPhenotypic switching of vascular smooth muscle cellsSwitching of vascular smooth muscle cellsNecrotic core areaRegulate vascular functionFoam cell populationVisceral myopathyBladder remodelingAortic atheromaFibrous cap thicknessRemodeling in vivoLipid malabsorptionVascular toneAbundant cell type
2024
Targeting USP25 in the Heart A Promising Therapeutic Strategy for Obesity-Associated Heart Disease?
Zhang H. Targeting USP25 in the Heart A Promising Therapeutic Strategy for Obesity-Associated Heart Disease? JACC Basic To Translational Science 2024, 9: 1305-1307. PMID: 39619142, PMCID: PMC11604408, DOI: 10.1016/j.jacbts.2024.08.001.Peer-Reviewed Original ResearchmiR-33 deletion in hepatocytes attenuates NAFLD-NASH-HCC progression
Fernández-Tussy P, Cardelo M, Zhang H, Sun J, Price N, Boutagy N, Goedeke L, Cadena-Sandoval M, Xirouchaki C, Brown W, Yang X, Pastor-Rojo O, Haeusler R, Bennett A, Tiganis T, Suárez Y, Fernández-Hernando C. miR-33 deletion in hepatocytes attenuates NAFLD-NASH-HCC progression. JCI Insight 2024, 9: e168476. PMID: 39190492, PMCID: PMC11466198, DOI: 10.1172/jci.insight.168476.Peer-Reviewed Original ResearchMiR-33Regulation of biological processesMitochondrial fatty acid oxidationRegulation of lipid metabolismNon-alcoholic fatty liver diseaseDevelopment of effective therapeuticsFatty acid oxidationLipid synthesisProgression of non-alcoholic fatty liver diseaseMitochondrial functionTarget genesBiological processesComplex diseasesNon-alcoholic steatohepatitisLipid accumulationDeletionDevelopment of non-alcoholic fatty liver diseasePathway activationLipid metabolismProgress to non-alcoholic steatohepatitisAcid oxidationHCC progressionEffective therapeuticsTherapeutic targetHepatocellular carcinomaAbstract 129: Hypercholesterolemia-induced Lxr Signaling In Smc Contributes To Atherosclerotic Lesion Remodeling And Regulates Vascular And Visceral Smc Function
Zhang H, Biwer L, de Urturi D, Fernandez-Tussy P, Jovin D, Huang Y, Zhang X, Esplugues E, Greif D, Suarez Y, Fernandez-Hernando C. Abstract 129: Hypercholesterolemia-induced Lxr Signaling In Smc Contributes To Atherosclerotic Lesion Remodeling And Regulates Vascular And Visceral Smc Function. Arteriosclerosis Thrombosis And Vascular Biology 2024, 44: a129-a129. DOI: 10.1161/atvb.44.suppl_1.129.Peer-Reviewed Original ResearchLiver X receptorTranscription factorsVascular smooth muscle cellsRegulation of lipid metabolismLXR signalingB geneScRNA-seqFate decisionsSignaling eventsSMC functionGene expressionActivation of liver X receptorCell statesLesion remodelingCharacterized miceLipid metabolismLineage tracingPhenotypic switchingX receptorReduced fibrous cap thicknessTranscriptionFeatures of plaque instabilitySmooth muscle cellsLipid absorptionProgression of atherosclerosisHeterogeneity of hepatocyte dynamics restores liver architecture after chemical, physical or viral damage
Ruz-Maldonado I, Gonzalez J, Zhang H, Sun J, Bort A, Kabir I, Kibbey R, Suárez Y, Greif D, Fernández-Hernando C. Heterogeneity of hepatocyte dynamics restores liver architecture after chemical, physical or viral damage. Nature Communications 2024, 15: 1247. PMID: 38341404, PMCID: PMC10858916, DOI: 10.1038/s41467-024-45439-0.Peer-Reviewed Original ResearchDynamic metabolism of endothelial triglycerides protects against atherosclerosis in mice
Boutagy N, Gamez-Mendez A, Fowler J, Zhang H, Chaube B, Esplugues E, Kuo A, Lee S, Horikami D, Zhang J, Citrin K, Singh A, Coon B, Lee M, Suarez Y, Fernandez-Hernando C, Sessa W. Dynamic metabolism of endothelial triglycerides protects against atherosclerosis in mice. Journal Of Clinical Investigation 2024, 134: e170453. PMID: 38175710, PMCID: PMC10866653, DOI: 10.1172/jci170453.Peer-Reviewed Original Research
2023
Proteomic profiling demonstrates inflammatory and endotheliopathy signatures associated with impaired cardiopulmonary exercise hemodynamic profile in Post Acute Sequelae of SARS‐CoV‐2 infection (PASC) syndrome
Singh I, Leitner B, Wang Y, Zhang H, Joseph P, Lutchmansingh D, Gulati M, Possick J, Damsky W, Hwa J, Heerdt P, Chun H. Proteomic profiling demonstrates inflammatory and endotheliopathy signatures associated with impaired cardiopulmonary exercise hemodynamic profile in Post Acute Sequelae of SARS‐CoV‐2 infection (PASC) syndrome. Pulmonary Circulation 2023, 13: e12220. PMID: 37091121, PMCID: PMC10113513, DOI: 10.1002/pul2.12220.Peer-Reviewed Original ResearchInvasive cardiopulmonary exercise testPASC patientsPost-acute sequelaeAcute sequelaeInfection syndromeUnexplained exertional intoleranceCardiopulmonary exercise testSystemic oxygen deliveryPersistent inflammatory stateVenous blood plasmaExertional intolerancePeak exerciseEndothelial dysfunctionHemodynamic profileInflammatory stateExercise testFibrotic processPathophysiological hallmarkAberrant protein expressionExpression of proteinsOxygen deliveryOxygen extractionProteomic profilingPatientsPhysiologic responses
2021
Increased complement activation is a distinctive feature of severe SARS-CoV-2 infection
Ma L, Sahu S, Cano M, Kuppuswamy V, Bajwa J, McPhatter J, Pine A, Meizlish M, Goshua G, Chang C, Zhang H, Price C, Bahel P, Rinder H, Lei T, Day A, Reynolds D, Wu X, Schriefer R, Rauseo A, Goss C, O’Halloran J, Presti R, Kim A, Gelman A, Dela Cruz C, Lee A, Mudd P, Chun H, Atkinson J, Kulkarni H. Increased complement activation is a distinctive feature of severe SARS-CoV-2 infection. Science Immunology 2021, 6: eabh2259. PMID: 34446527, PMCID: PMC8158979, DOI: 10.1126/sciimmunol.abh2259.Peer-Reviewed Original ResearchConceptsSevere SARS-CoV-2 infectionSARS-CoV-2 infectionIntensive care unitComplement activationRespiratory failureEndothelial injuryCOVID-19Non-COVID cohortPersonalized clinical trialsAcute respiratory failureInvasive mechanical ventilationSevere COVID-19Tertiary care centerAlternative complement pathwayICU admissionCritical illnessCare unitMechanical ventilationRisk prognosticationWashington University SchoolWorse outcomesCare centerClinical trialsHigh riskPatientsPRO-THROMBOTIC SIGNATURE FROM NEUTROPHIL ACTIVATION AND DECREASED ADAMTS13 TO VWF RATIO IS A KEY DRIVER OF CARDIAC INJURY IN HOSPITALIZED PATIENTS WITH COVID-19
Wang S, Pine A, Mankbadi M, Chang C, Madeeva D, Zhang H, Dajani A, Crandall I, Sugeng L, Lee A, Chun H. PRO-THROMBOTIC SIGNATURE FROM NEUTROPHIL ACTIVATION AND DECREASED ADAMTS13 TO VWF RATIO IS A KEY DRIVER OF CARDIAC INJURY IN HOSPITALIZED PATIENTS WITH COVID-19. Journal Of The American College Of Cardiology 2021, 77: 3193. PMID: 34167644, PMCID: PMC8091195, DOI: 10.1016/s0735-1097(21)04548-4.Peer-Reviewed Original Research
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