2022
Brown adipose TRX2 deficiency activates mtDNA-NLRP3 to impair thermogenesis and protect against diet-induced insulin resistance
Huang Y, Zhou JH, Zhang H, Canfrán-Duque A, Singh AK, Perry RJ, Shulman G, Fernandez-Hernando C, Min W. Brown adipose TRX2 deficiency activates mtDNA-NLRP3 to impair thermogenesis and protect against diet-induced insulin resistance. Journal Of Clinical Investigation 2022, 132 PMID: 35202005, PMCID: PMC9057632, DOI: 10.1172/jci148852.Peer-Reviewed Original ResearchConceptsBrown adipose tissueBAT inflammationInsulin resistanceMitochondrial reactive oxygen speciesReactive oxygen speciesAberrant innate immune responsesDiet-induced insulin resistanceSystematic metabolismDiet-induced obesityNLRP3 inflammasome pathwayWhole-body energy metabolismCGAS/STINGInnate immune responseFatty acid oxidationExcessive mitochondrial reactive oxygen speciesMetabolic benefitsImmune responseInflammasome pathwayAdipose tissueInflammationInhibition reversesLipid uptakeLipid metabolismThioredoxin 2Adaptive thermogenesis
2020
Mitophagy-mediated adipose inflammation contributes to type 2 diabetes with hepatic insulin resistance
He F, Huang Y, Song Z, Zhou HJ, Zhang H, Perry RJ, Shulman GI, Min W. Mitophagy-mediated adipose inflammation contributes to type 2 diabetes with hepatic insulin resistance. Journal Of Experimental Medicine 2020, 218: e20201416. PMID: 33315085, PMCID: PMC7927432, DOI: 10.1084/jem.20201416.Peer-Reviewed Original ResearchMeSH KeywordsAdipocytesAdipose TissueAnimalsDiabetes Mellitus, Type 2Diet, High-FatEnergy MetabolismFatty LiverGene DeletionGene TargetingGluconeogenesisHomeostasisHumansHyperglycemiaInflammationInsulin ResistanceLipogenesisLiverMaleMice, Inbred C57BLMice, KnockoutMitochondriaMitophagyNF-kappa BOxidative StressPhenotypeReactive Oxygen SpeciesSequestosome-1 ProteinSignal TransductionThioredoxinsConceptsHepatic insulin resistanceWhite adipose tissueInsulin resistanceAdipose inflammationType 2 diabetes mellitusLipid metabolic disordersNF-κB inhibitorAdipose-specific deletionWhole-body energy homeostasisAltered fatty acid metabolismFatty acid metabolismT2DM progressionT2DM patientsDiabetes mellitusReactive oxygen species pathwayHepatic steatosisMetabolic disordersNF-κBP62/SQSTM1Adipose tissueHuman adipocytesEnergy homeostasisExcessive mitophagyOxygen species pathwayInflammation
2015
SENP1-mediated NEMO deSUMOylation in adipocytes limits inflammatory responses and type-1 diabetes progression
Shao L, Zhou HJ, Zhang H, Qin L, Hwa J, Yun Z, Ji W, Min W. SENP1-mediated NEMO deSUMOylation in adipocytes limits inflammatory responses and type-1 diabetes progression. Nature Communications 2015, 6: 8917. PMID: 26596471, PMCID: PMC4662081, DOI: 10.1038/ncomms9917.Peer-Reviewed Original ResearchMeSH Keywords3T3-L1 CellsAdipocytesAnimalsApoptosisChemokine CCL5Chromatin ImmunoprecipitationCysteine EndopeptidasesCytokinesDiabetes Mellitus, Type 1Diabetes Mellitus, Type 2Diet, High-FatEndopeptidasesEnzyme-Linked Immunosorbent AssayFlow CytometryGene Knockout TechniquesGlucose IntoleranceHyperglycemiaImmunoblottingImmunoprecipitationInflammationInsulin ResistanceInsulin-Secreting CellsIntracellular Signaling Peptides and ProteinsIslets of LangerhansMiceMutagenesis, Site-DirectedNF-kappa BPhenotypeReverse Transcriptase Polymerase Chain ReactionSmall Ubiquitin-Related Modifier ProteinsConceptsNF-κB activityAdipocyte dysfunctionCytokine productionType 1 diabetes progressionPancreatic isletsType 1 diabetes mellitusMild insulin resistanceDevelopment of diabetesType 2 diabetes phenotypeΒ-cell damageDirect cytotoxic effectNF-κB inhibitorAdipocyte-specific deletionProgression of T1DMDiabetes mellitusGlucose intolerancePancreatic inflammationProinflammatory cytokinesCCL5 expressionInsulin resistanceDiabetes progressionInflammatory responseNF-κBDiabetes phenotypeMice exhibit
2013
AIP1 Suppresses Atherosclerosis by Limiting Hyperlipidemia-Induced Inflammation and Vascular Endothelial Dysfunction
Huang Q, Qin L, Dai S, Zhang H, Pasula S, Zhou H, Chen H, Min W. AIP1 Suppresses Atherosclerosis by Limiting Hyperlipidemia-Induced Inflammation and Vascular Endothelial Dysfunction. Arteriosclerosis Thrombosis And Vascular Biology 2013, 33: 795-804. PMID: 23413429, PMCID: PMC3637885, DOI: 10.1161/atvbaha.113.301220.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAortic DiseasesApolipoproteins EAtherosclerosisBiomarkersBone Marrow TransplantationCholesterolCytokinesDisease Models, AnimalDose-Response Relationship, DrugEndothelium, VascularGene Expression RegulationHyperlipidemiasInflammationInflammation MediatorsLipoproteinsLipoproteins, LDLMacrophagesMiceMice, KnockoutNF-kappa BRas GTPase-Activating ProteinsSignal TransductionTriglyceridesVasoconstrictionVasoconstrictor AgentsVasodilationVasodilator AgentsConceptsInflammatory responseAtherosclerotic lesionsAortic ECsNuclear factor-κB (NF-κB) activityVascular endothelial dysfunctionPlasma inflammatory cytokinesWestern-type dietTotal cholesterol levelsIncreased inflammatory responseNuclear factor-κB signalingEndothelial cell dysfunctionAccumulation of macrophagesDouble knockout miceFactor-κB signalingNull mouse modelEndothelial dysfunctionProinflammatory mediatorsSuppresses AtherosclerosisControl miceInflammatory moleculesLipoprotein profileInflammatory cytokinesCholesterol levelsAortic rootEC dysfunction
2008
AIP1 functions as an endogenous inhibitor of VEGFR2-mediated signaling and inflammatory angiogenesis in mice
Zhang H, He Y, Dai S, Xu Z, Luo Y, Wan T, Luo D, Jones D, Tang S, Chen H, Sessa WC, Min W. AIP1 functions as an endogenous inhibitor of VEGFR2-mediated signaling and inflammatory angiogenesis in mice. Journal Of Clinical Investigation 2008, 118: 3904-3916. PMID: 19033661, PMCID: PMC2575835, DOI: 10.1172/jci36168.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCattleCell MovementCorneal NeovascularizationDisease Models, AnimalEndothelial CellsHumansInflammationMiceMice, KnockoutNeovascularization, PathologicOrgan SpecificityPhosphatidylinositol 3-KinasesRas GTPase-Activating ProteinsSignal TransductionVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2ConceptsASK1-interacting protein-1Inflammatory angiogenesisKO miceEndogenous inhibitorInhibition of VEGFR2PI3K p85Retina neovascularizationAdaptive angiogenesisVEGF-VEGFR2 signalingRetinal angiogenesisEC migrationMiceVascular ECsVEGF responseAngiogenesisProtein 1EC apoptosisVEGFR2Late phaseVEGFMechanistic dataVascular developmentAIP1 functionsK-complexesInhibitors
2006
SOCS1 Inhibits Tumor Necrosis Factor-induced Activation of ASK1-JNK Inflammatory Signaling by Mediating ASK1 Degradation*
He Y, Zhang W, Zhang R, Zhang H, Min W. SOCS1 Inhibits Tumor Necrosis Factor-induced Activation of ASK1-JNK Inflammatory Signaling by Mediating ASK1 Degradation*. Journal Of Biological Chemistry 2006, 281: 5559-5566. PMID: 16407264, DOI: 10.1074/jbc.m512338200.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCattleCells, CulturedEndothelial CellsEnzyme ActivationInflammationIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesMAP Kinase Kinase Kinase 5MiceMice, KnockoutRecombinant Fusion ProteinsRepressor ProteinsSignal TransductionSrc Homology DomainsSuppressor of Cytokine Signaling 1 ProteinSuppressor of Cytokine Signaling 3 ProteinSuppressor of Cytokine Signaling ProteinsTumor Necrosis Factor-alphaConceptsASK1 degradationDissociation of ASK1Member of suppressorTumor necrosis factor-induced activationEndothelial cellsActivation of JNKPhosphotyrosine bindingUndergoes ubiquitinationSH2 domainProteasomal inhibitorsASK1 activationNegative regulatorApoptotic responseASK1Cytokine signalingSOCS1 functionsASK1 expressionSOCS1Tumor necrosis factorSignalingSOCS1-deficient mice