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