2025
Modulation of the thiol redox proteome by sugarcane ash-derived silica nanoparticles: insights into chronic kidney disease of unknown etiology
Stem A, Michel C, Harris P, Rogers K, Gibb M, Roncal-Jimenez C, Reisdorph R, Johnson R, Roede J, Fritz K, Brown J. Modulation of the thiol redox proteome by sugarcane ash-derived silica nanoparticles: insights into chronic kidney disease of unknown etiology. Particle And Fibre Toxicology 2025, 22: 3. PMID: 39910563, PMCID: PMC11800628, DOI: 10.1186/s12989-025-00619-8.Peer-Reviewed Original ResearchMeSH KeywordsBasic Helix-Loop-Helix Transcription FactorsCell LineChronic Kidney Diseases of Uncertain EtiologyHumansKidney Tubules, ProximalNanoparticlesOccupational ExposureOxidation-ReductionOxidative StressProteomeProteomicsReactive Oxygen SpeciesReceptors, Aryl HydrocarbonRenal Insufficiency, ChronicSaccharumSilicon DioxideSulfhydryl CompoundsConceptsProximal convoluted tubulesActivation of aryl hydrocarbon receptorExposure to silica nanoparticlesDisease of unknown etiologyReactive oxygen speciesKidney proximal convoluted tubuleIncreased reactive oxygen species generationChronic kidney diseaseSignaling pathwayIntroductionChronic kidney diseaseHK-2 cellsReactive oxygen species generationProfile in vitroPotential mechanisms of toxicityMembrane hyperpolarizationCKD progressionUnknown etiologyGeneration of reactive oxygen speciesMitochondrial membrane hyperpolarizationOxygen species generationAryl hydrocarbon receptorEnergy metabolismKidney diseaseConvoluted tubulesMechanisms of toxicity
2024
Balanced regulation of ROS production and inflammasome activation in preventing early development of colorectal cancer
Li L, Xu T, Qi X. Balanced regulation of ROS production and inflammasome activation in preventing early development of colorectal cancer. Immunological Reviews 2024, 329: e13417. PMID: 39523732, DOI: 10.1111/imr.13417.Peer-Reviewed Original ResearchRegulation of ROS productionBalanced ROS productionReactive oxygen speciesROS productionColitis-associated colorectal cancerInflammasome activationColorectal cancerInnate immune response to microbial infectionResponse to microbial infectionImmune response to microbial infectionReactive oxygen species sensorSource of ROS productionCell-cell contactNADPH oxidase complexInflammasome activation studiesReactive oxygen species generationASC speck formationBalance regulationCrohn's diseaseSignaling networksROS signalingSusceptibility genesNADPH complexPerinuclear regionSterile insults
2023
Functions of Peroxiredoxins and Their Roles in Autoimmune Diseases
Zhou F, Chen F, Ouyang Z, Zhu R, Zhou R, Hu W, Lu C. Functions of Peroxiredoxins and Their Roles in Autoimmune Diseases. Antioxidants And Redox Signaling 2023, 40: 329-344. PMID: 36738225, DOI: 10.1089/ars.2022.0139.Peer-Reviewed Original ResearchFunction of peroxiredoxinsAutoimmune diseasesCellular redox signalingOxidative stressRedox signalingRedox homeostasisEssential regulatorExcess ROSPeroxiredoxinsBiological processesReactive oxygen species generationProduction of ROSPhysiological roleNew therapeutic targetsOxygen species generationAntioxidant enzymesPotential targetPathophysiological rolePathological situationsEffective treatmentTherapeutic targetSpecies generationDiseaseROSRecent studies
2021
Comprehensive review on ultrasound-responsive theranostic nanomaterials: mechanisms, structures and medical applications
Fateh S, Moradi L, Kohan E, Hamblin M, Dezfuli A. Comprehensive review on ultrasound-responsive theranostic nanomaterials: mechanisms, structures and medical applications. Beilstein Journal Of Nanotechnology 2021, 12: 808-862. PMID: 34476167, PMCID: PMC8372309, DOI: 10.3762/bjnano.12.64.Peer-Reviewed Original ResearchTheranostic nanomaterialsCell deathReactive oxygen species generationClinical imaging modalitiesOxygen species generationTherapeutic effectImaging modalitiesMesoporous silica nanoparticlesPolymeric nanoparticlesRelease of encapsulated drugsAcoustic radiation forceTitania nanostructuresSpecies generationCarbon nanostructuresLocal thermal effectsUltrasoundDroplet vaporizationSilica nanoparticlesAcoustic droplet vaporizationCavitation microbubblesDeathTheranosticsThermal effectsNanoparticlesNanomaterialsBBIT20 inhibits homologous DNA repair with disruption of the BRCA1–BARD1 interaction in breast and ovarian cancer
Raimundo L, Paterna A, Calheiros J, Ribeiro J, Cardoso DSP, Piga I, Neto SJ, Hegan D, Glazer PM, Indraccolo S, Mulhovo S, Costa JL, Ferreira M, Saraiva L. BBIT20 inhibits homologous DNA repair with disruption of the BRCA1–BARD1 interaction in breast and ovarian cancer. British Journal Of Pharmacology 2021, 178: 3627-3647. PMID: 33899955, PMCID: PMC9124438, DOI: 10.1111/bph.15506.Peer-Reviewed Original ResearchConceptsTriple-negative breastOvarian cancerXenograft mouse modelMouse modelAntitumour activityAdvanced ovarian cancerCancer cellsPatient-derived cell linesHomologous DNA repairOvarian cancer cellsNon-malignant cellsPatient-derived cellsMarked synergistic effectAvailable therapiesCombination therapyCell cycle arrestReactive oxygen species generationSide effectsDNA repair-related genesSingle agentTherapeutic outcomesCancerOxygen species generationPersonalized treatmentResistant cancers
2019
Short AIP1 (ASK1-Interacting Protein-1) Isoform Localizes to the Mitochondria and Promotes Vascular Dysfunction
Li Z, Li L, Zhang H, Zhou HJ, Ji W, Min W. Short AIP1 (ASK1-Interacting Protein-1) Isoform Localizes to the Mitochondria and Promotes Vascular Dysfunction. Arteriosclerosis Thrombosis And Vascular Biology 2019, 40: 112-127. PMID: 31619063, PMCID: PMC7204498, DOI: 10.1161/atvbaha.119.312976.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAorta, ThoracicApoptosisArteriosclerosisBlotting, WesternCells, CulturedDisease Models, AnimalDNAEndothelium, VascularGene Expression RegulationGenome-Wide Association StudyHumansMiceMice, Inbred C57BLMice, TransgenicMicroscopy, FluorescenceMitochondriaras GTPase-Activating ProteinsSignal TransductionConceptsN-terminal pleckstrin homology domainHuman genome-wide association studiesGenome-wide association studiesPleckstrin homology domainMitochondrial reactive oxygen species generationEndothelial cellsH3K9 trimethylationHomology domainReactive oxygen species productionOxygen species productionReactive oxygen speciesReactive oxygen species generationAssociation studiesRegulatory factorsEpigenetic inhibitionEC activationOxygen species generationDependent pathwayVascular endothelial cellsProteolytic degradationSpecies productionOxygen speciesVascular homeostasisMitochondriaSpecies generation
2017
Pro-inflammatory hepatic macrophages generate ROS through NADPH oxidase 2 via endocytosis of monomeric TLR4–MD2 complex
Kim S, Jeong J, Kim S, Seo W, Kim M, Choi W, Yoo W, Lee J, Shim Y, Yi H, Lee Y, Eun H, Lee B, Chun K, Kang S, Kim S, Gao B, Kunos G, Kim H, Jeong W. Pro-inflammatory hepatic macrophages generate ROS through NADPH oxidase 2 via endocytosis of monomeric TLR4–MD2 complex. Nature Communications 2017, 8: 2247. PMID: 29269727, PMCID: PMC5740170, DOI: 10.1038/s41467-017-02325-2.Peer-Reviewed Original ResearchConceptsEndocytosis of TLR4Reactive oxygen speciesReactive oxygen species generationTLR4-MD2 complexDynamin-mediated endocytosisInhibition of dynaminHigh-fat diet-induced hepatic steatosisDiet-induced hepatic steatosisNADPH oxidaseTriggering endocytosisNon-alcoholic fatty liver diseaseEndocytosisROS generationDevelopment of non-alcoholic fatty liver diseaseFatty liver diseaseNADPH oxidase 2Oxygen speciesTLR4-MD2Toll-like receptor 4Multiple mechanismsTherapeutic targetNADPHHepatic steatosisInfiltrating MacrophagesDynaminMechanistic Role of Thioredoxin 2 in Heart Failure
Chen C, Chen H, Zhou HJ, Ji W, Min W. Mechanistic Role of Thioredoxin 2 in Heart Failure. Advances In Experimental Medicine And Biology 2017, 982: 265-276. PMID: 28551792, DOI: 10.1007/978-3-319-55330-6_14.Peer-Reviewed Original ResearchConceptsThioredoxin 2ASK1-dependent apoptosisMechanistic roleMitochondrial reactive oxygen species generationCellular oxidative stressGlobal gene knockoutMitochondrial proteinsEmbryonic lethalityMitochondrial Trx2Gene knockoutKinase 1Reactive oxygen species generationTrx2Key mechanistic roleOxygen species generationCardiomyocyte apoptosisActive tissuesApoptosisCommon mechanismOxidative stressSpecies generationPromising targetHeart failureTherapeutic strategiesTreatment of DCM
2016
Soluble Receptor for Advanced Glycation End Products Improves Stromal Cell–Derived Factor-1 Activity in Model Diabetic Environments
Olekson MP, Faulknor RA, Hsia HC, Schmidt AM, Berthiaume F. Soluble Receptor for Advanced Glycation End Products Improves Stromal Cell–Derived Factor-1 Activity in Model Diabetic Environments. Advances In Wound Care 2016, 5: 527-538. PMID: 28078186, PMCID: PMC5165672, DOI: 10.1089/wound.2015.0674.Peer-Reviewed Original ResearchStromal cell-derived factor-1Advanced glycation end productsPeripheral blood mononuclear cellsCellular responsesSoluble RAGEGlycation end productsBaseline ROS levelsGrowth factorExtracellular signalsExogenous SDF-1Mouse peripheral blood mononuclear cellsStem cell recruitmentHuman leukaemia 60 cellsCell-derived factor-1Exogenous growth factorsReactive oxygen species generationDiabetic murine woundsReceptor CXCR-4Blood mononuclear cellsWound healingCellular migrationCell migrationOxygen species generationMurine excisional wound modelROS levelsMitochondrial Redox Signaling and Tumor Progression
Chen Y, Zhang H, Zhou HJ, Ji W, Min W. Mitochondrial Redox Signaling and Tumor Progression. Cancers 2016, 8: 40. PMID: 27023612, PMCID: PMC4846849, DOI: 10.3390/cancers8040040.Peer-Reviewed Original ResearchMitochondrial redox proteinsExcessive ROSRedox proteinsCancer cellsMitochondrial redox signalingMitochondrial oxidative phosphorylationCellular ROS levelsStress signalingRedox regulationROS functionTumor progressionRedox signalingMitochondrial roleApoptotic signalingCancer cell proliferationRedox-sensitive pathwaysTranscriptional factorsReactive oxygen species generationTumor suppressorOxidative phosphorylationDNA mutationsOxygen species generationCancer progressionBasal ROSCancer invasion
2015
Thioredoxin-2 Inhibits Mitochondrial Reactive Oxygen Species Generation and Apoptosis Stress Kinase-1 Activity to Maintain Cardiac Function
Huang Q, Zhou HJ, Zhang H, Huang Y, Hinojosa-Kirschenbaum F, Fan P, Yao L, Belardinelli L, Tellides G, Giordano FJ, Budas GR, Min W. Thioredoxin-2 Inhibits Mitochondrial Reactive Oxygen Species Generation and Apoptosis Stress Kinase-1 Activity to Maintain Cardiac Function. Circulation 2015, 131: 1082-1097. PMID: 25628390, PMCID: PMC4374031, DOI: 10.1161/circulationaha.114.012725.Peer-Reviewed Original ResearchConceptsMitochondrial reactive oxygen species generationReactive oxygen species generationOxygen species generationASK1-dependent apoptosisMitochondrial reactive oxygen species productionPhosphorylation/activityKey mitochondrial proteinsSpecies generationMitochondrial membrane depolarizationKinase 1 activityMitochondrial proteinsReactive oxygen species productionCellular redoxMitochondrial Trx2Inhibition of ASK1Apoptotic signalingOxygen species productionThioredoxin 2Protein expression levelsKinase 1ATP productionASK1 inhibitionKnockout miceMitochondrial ultrastructureASK1 inhibitors
2014
Long-Acting Progestin-Only Contraceptives Enhance Human Endometrial Stromal Cell Expressed Neuronal Pentraxin-1 and Reactive Oxygen Species to Promote Endothelial Cell Apoptosis
Guzeloglu-Kayisli O, Basar M, Shapiro J, Semerci N, Huang J, Schatz F, Lockwood C, Kayisli U. Long-Acting Progestin-Only Contraceptives Enhance Human Endometrial Stromal Cell Expressed Neuronal Pentraxin-1 and Reactive Oxygen Species to Promote Endothelial Cell Apoptosis. The Journal Of Clinical Endocrinology & Metabolism 2014, 99: e1957-e1966. PMID: 25029423, PMCID: PMC4184079, DOI: 10.1210/jc.2014-1770.Peer-Reviewed Original ResearchMeSH KeywordsApoptosisC-Reactive ProteinCaspase 3Cell ProliferationCells, CulturedContraceptive Agents, FemaleCulture Media, ConditionedCytochromes cEndometriumEndothelial CellsEstradiolFemaleHumansMedroxyprogesterone AcetateMicrovesselsNerve Tissue ProteinsParacrine CommunicationProgestinsReactive Oxygen SpeciesStromal CellsConceptsHuman endometrial endothelial cellsNeuronal pentraxin 1Abnormal uterine bleedingUterine bleedingMedroxyprogesterone acetateReactive oxygen species generationCultured human endometrial endothelial cellsOxygen species generationHuman endometrial stromal cellsUterine blood flowEndometrium of womenEndometrial endothelial cellsEndometrial stromal cellsProgesterone receptor proteinCaspase-3Elevated reactive oxygen species (ROS) generationHESC-CMsNovel paracrine mechanismEndothelial cell apoptosisSpecies generationFragile microvesselsCytosolic cytochrome c levelsParacrine mechanismsBlood flowLAPCThe Mitochondrial Cardiolipin Remodeling Enzyme Lysocardiolipin Acyltransferase Is a Novel Target in Pulmonary Fibrosis
Huang LS, Mathew B, Li H, Zhao Y, Ma SF, Noth I, Reddy SP, Harijith A, Usatyuk PV, Berdyshev EV, Kaminski N, Zhou T, Zhang W, Zhang Y, Rehman J, Kotha SR, Gurney TO, Parinandi NL, Lussier YA, Garcia JG, Natarajan V. The Mitochondrial Cardiolipin Remodeling Enzyme Lysocardiolipin Acyltransferase Is a Novel Target in Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2014, 189: 1402-1415. PMID: 24779708, PMCID: PMC4098083, DOI: 10.1164/rccm.201310-1917oc.Peer-Reviewed Original ResearchMeSH Keywords1-Acylglycerol-3-Phosphate O-AcyltransferaseAcyltransferasesAnimalsBiomarkersCardiolipinsCohort StudiesDisease Models, AnimalHumansIdiopathic Pulmonary FibrosisIn Situ HybridizationLeukocytes, MononuclearMiceMitochondriaPredictive Value of TestsPulmonary FibrosisRNA, MessengerSensitivity and SpecificitySeverity of Illness IndexConceptsPeripheral blood mononuclear cellsIdiopathic pulmonary fibrosisPulmonary fibrosisMurine modelAlveolar epithelial cellsOverall survivalReactive oxygen species generationLysocardiolipin acyltransferaseOxygen species generationCarbon monoxide diffusion capacityRadiation-induced pulmonary fibrosisPulmonary function outcomesEpithelial cellsBlood mononuclear cellsPreclinical murine modelsNovel therapeutic approachesSpecies generationBleomycin challengeLung inflammationLung protectionPulmonary functionFunction outcomesLung fibrosisMononuclear cellsFibrotic lungs
2013
Mitochondria and AMP-activated Protein Kinase-dependent Mechanism of Efferocytosis*
Jiang S, Park D, Stigler W, Creighton J, Ravi S, Darley-Usmar V, Zmijewski J. Mitochondria and AMP-activated Protein Kinase-dependent Mechanism of Efferocytosis*. Journal Of Biological Chemistry 2013, 288: 26013-26026. PMID: 23897815, PMCID: PMC3764806, DOI: 10.1074/jbc.m113.489468.Peer-Reviewed Original ResearchConceptsActivation of AMP-activated kinaseApoptotic cellsAMPK activationAMP-activated protein kinase-dependent mechanismRemoval of apoptotic cellsMitochondrial reactive oxygen species generationAMP-activated kinaseClearance of apoptotic cellsInhibition of mitochondrial oxygen consumptionExposure to apoptotic cellsUptake of apoptotic cellsDefective clearance of apoptotic cellsReactive oxygen species generationMitochondrial oxygen consumptionATP productionThymocytes in vitroOxygen species generationMicrotubule synthesisTissue homeostasisDying CellsDefective clearanceReturn to tissue homeostasisSpecies generationCa(2+Cells
2010
P‐Rex1 regulates lung microvascular permeability
Naikawadi R, Cheng N, Wu D, Ye R. P‐Rex1 regulates lung microvascular permeability. The FASEB Journal 2010, 24: lb554-lb554. DOI: 10.1096/fasebj.24.1_supplement.lb554.Peer-Reviewed Original ResearchAcute lung injuryLung microvascular permeabilityPolymorphonuclear leukocytesLung injuryEndothelial cellsP-Rex1 expressionMicrovascular permeabilityLung microvascular endothelial cellsGram-negative bacterial infectionsTNF-alpha contributesWild-type miceMicrovascular endothelial cellsEndothelial barrier permeabilityP-Rex1Endothelial cell signalingBacterial clearanceTNF-alphaReactive oxygen species generationBarrier permeabilityType miceMajor cytokineKnockout miceBacterial infectionsSepticemic infectionUncontrolled activation
2003
Modulation of mitochondrial function by endogenous Zn2+ pools
Sensi SL, Ton-That D, Sullivan PG, Jonas EA, Gee KR, Kaczmarek LK, Weiss JH. Modulation of mitochondrial function by endogenous Zn2+ pools. Proceedings Of The National Academy Of Sciences Of The United States Of America 2003, 100: 6157-6162. PMID: 12724524, PMCID: PMC156342, DOI: 10.1073/pnas.1031598100.Peer-Reviewed Original ResearchConceptsDirect patch-clamp recordingsCultured cortical neuronsPatch-clamp recordingsCertain brain regionsNeuronal injuryPool of intracellularCortical neuronsIntact neuronsReactive oxygen species generationPostsynaptic neuronsClamp recordingsSynaptic spacePotent effectsBrain regionsOxygen species generationBrain mitochondriaMitochondrial poolMembrane depolarizationNeuronsRecent evidenceFurther studiesMitochondrial functionROS generationNovel evidenceSpecies generation
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply