Hanming Zhang, PhD
Postdoctoral AssociateAbout
Titles
Postdoctoral Associate
Education & Training
- PhD
- University of South Dakota (2019)
- BS
- Zhejiang Sci-Tech University (2012)
Research
Publications
2024
Abstract 129: Hypercholesterolemia-induced Lxr Signaling In Smc Contributes To Atherosclerotic Lesion Remodeling And Regulates Vascular And Visceral Smc Function
Zhang H, Biwer L, Saenz 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 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 ResearchA 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 ResearchConceptsCritical 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
Circulating markers of angiogenesis and endotheliopathy in COVID‐19
Pine AB, Meizlish ML, Goshua G, Chang C, Zhang H, Bishai J, Bahel P, Patel A, Gbyli R, Kwan JM, Won CH, Price C, Dela Cruz CS, Halene S, van Dijk D, Hwa J, Lee AI, Chun HJ. Circulating markers of angiogenesis and endotheliopathy in COVID‐19. Pulmonary Circulation 2020, 10: 1-4. PMID: 33282193, PMCID: PMC7691906, DOI: 10.1177/2045894020966547.Peer-Reviewed Original ResearchCOVID-19 infectionMarkers of angiogenesisEndothelial injuryDisease severityCOVID-19-associated coagulopathyCritical COVID-19 infectionCOVID-19 pathogenesisCOVID-19COVID-19 diseaseEndothelial cell functionHospital mortalityMicrovascular complicationsCritical illnessElevated markersHospitalized patientsPatient populationFuture therapiesPlasma profilingSurvival analysisPatientsInfectionCell functionPotential targetInjuryMarkersEndotheliopathy 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 ResearchMeSH 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
2019
PDE1 inhibition facilitates proteasomal degradation of misfolded proteins and protects against cardiac proteinopathy
Zhang H, Pan B, Wu P, Parajuli N, Rekhter MD, Goldberg AL, Wang X. PDE1 inhibition facilitates proteasomal degradation of misfolded proteins and protects against cardiac proteinopathy. Science Advances 2019, 5: eaaw5870. PMID: 31131329, PMCID: PMC6531002, DOI: 10.1126/sciadv.aaw5870.Peer-Reviewed Original ResearchMeSH KeywordsAlpha-Crystallin B ChainAnimalsCyclic AMP-Dependent Protein KinasesCyclic GMP-Dependent Protein KinasesCyclic Nucleotide Phosphodiesterases, Type 1DensitometryEchocardiographyFemaleGenotypeHeart FailureHeart VentriclesHemodynamicsHumansHydrolysisMaleMiceMice, TransgenicMicroscopy, FluorescenceMyocytes, CardiacPhosphorylationProteasome Endopeptidase ComplexProtein DenaturationProtein FoldingProteostasis DeficienciesRats
Academic Achievements and Community Involvement
Links & Media
News
- April 27, 2023
Study Uncovers Reduced Exercise Tolerance and Other Changes in Long COVID
- April 29, 2021
ACC 2021: Late-Breaking Studies Highlight New Treatment Protocols
- February 25, 2021
Blood Tests Offer Early Indicator of Severe COVID-19, Study Says
- June 30, 2020
Yale IDs Test to Detect Blood Vessel Injury, Predict Survival in COVID-19