2025
HIF-1α and VEGF Immunophenotypes as Potential Biomarkers in the Prognosis and Evaluation of Treatment Efficacy of Atherosclerosis: A Systematic Review of the Literature
Vageli D, Doukas P, Georgiou D, Prokopiou M, Ladaki N, Papadopoulou A, Doukas S, Zacharouli K, Makaritsis K, Ioannou M. HIF-1α and VEGF Immunophenotypes as Potential Biomarkers in the Prognosis and Evaluation of Treatment Efficacy of Atherosclerosis: A Systematic Review of the Literature. Frontiers In Bioscience-Landmark 2025, 30: 27004. PMID: 39862086, DOI: 10.31083/fbl27004.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAtherosclerosisBiomarkersHumansHypoxia-Inducible Factor 1, alpha SubunitImmunophenotypingMicroRNAsPlaque, AtheroscleroticPrognosisTreatment OutcomeVascular Endothelial Growth Factor AConceptsVascular endothelial growth factorTreatment efficacyHIF-1aUpregulation of pro-inflammatory moleculesPotential biomarkersMitogen-activated protein kinaseAttenuation of atherosclerosis progressionOverexpression of vascular endothelial growth factorVascular endothelial growth factor protein expressionIncreased VEGFVascular endothelial growth factor overexpressionLipopolysaccharide-induced tumor necrosis factor-alpha factorAtherosclerosis progressionSystematic reviewTumor necrosis factor-alphaVascular smooth muscle cellsExposure to methamphetamineAdenosine receptor antagonistHypoxia-inducible factor-1 alphaNecrosis factor-alphaNitric oxideChronic exposure to methamphetamineEndothelial growth factorSmooth muscle cellsEvaluation of treatment efficacy
2024
Targeting hypoxia and thrombospondin‐2 in diabetic wound healing
Huang Y, Xing H, Naud S, Kyriakides T. Targeting hypoxia and thrombospondin‐2 in diabetic wound healing. The FASEB Journal 2024, 38: e70091. PMID: 39383062, PMCID: PMC11486302, DOI: 10.1096/fj.202302429rrr.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acids, DicarboxylicAnimalsCell HypoxiaDiabetes Mellitus, ExperimentalFibroblastsHypoxiaHypoxia-Inducible Factor 1, alpha SubunitMaleMiceMice, Inbred C57BLMice, KnockoutThrombospondinsWound HealingConceptsThrombospondin-2Diabetic miceWound healingHIF-1aMatricellular protein thrombospondin-2Diabetic woundsImpaired wound healingWounds of diabetic miceDimethyloxalylglycine treatmentTargeting hypoxiaSustained hypoxiaDiabetic patientsTSP2 expressionCell dysfunctionIncreased neovascularizationDiabetic wound healingGenetic ablationDiabetic fibroblastsElevated glucoseReduced hypoxiaImprove healingImmunofluorescence analysisHIF-1a activationHypoxiaWestern blotting
2023
Mitochondrial leak metabolism induces the Spemann-Mangold Organizer via Hif-1α in Xenopus
MacColl Garfinkel A, Mnatsakanyan N, Patel J, Wills A, Shteyman A, Smith P, Alavian K, Jonas E, Khokha M. Mitochondrial leak metabolism induces the Spemann-Mangold Organizer via Hif-1α in Xenopus. Developmental Cell 2023, 58: 2597-2613.e4. PMID: 37673063, PMCID: PMC10840693, DOI: 10.1016/j.devcel.2023.08.015.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine TriphosphateAnimalsHypoxiaHypoxia-Inducible Factor 1, alpha SubunitMitochondriaOrganizers, EmbryonicXenopus laevisConceptsSpemann-Mangold organizerATP productionMitochondrial respirationC subunit ringHIF-1αMitochondrial oxidative metabolismEmbryonic patterningCell fateATP synthaseC subunitVentral mesodermHIF-1α activationInstructive roleHypoxia-inducible factor-1αΒ-cateninGeneral mechanismXenopusFactor-1αRespirationMembrane leakOxidative metabolismMetabolismMesodermActivationOxygen consumption
2022
Single cell transcriptomic landscape of diabetic foot ulcers
Theocharidis G, Thomas BE, Sarkar D, Mumme HL, Pilcher WJR, Dwivedi B, Sandoval-Schaefer T, Sîrbulescu RF, Kafanas A, Mezghani I, Wang P, Lobao A, Vlachos IS, Dash B, Hsia HC, Horsley V, Bhasin SS, Veves A, Bhasin M. Single cell transcriptomic landscape of diabetic foot ulcers. Nature Communications 2022, 13: 181. PMID: 35013299, PMCID: PMC8748704, DOI: 10.1038/s41467-021-27801-8.Peer-Reviewed Original ResearchMeSH KeywordsBiomarkersCell Adhesion MoleculesChitinase-3-Like Protein 1Diabetes MellitusDiabetic FootEndothelial CellsExome SequencingFibroblastsGene Expression RegulationHigh-Throughput Nucleotide SequencingHumansHypoxia-Inducible Factor 1, alpha SubunitKeratinocytesLeukocytesMacrophagesMatrix Metalloproteinase 1Matrix Metalloproteinase 11Matrix Metalloproteinase 3Single-Cell AnalysisSkinTranscriptomeWound HealingConceptsDiabetic foot ulcerationSpatial transcriptomicsSingle-cell transcriptomic landscapeSingle-cell RNA sequencingPeripheral blood mononuclear cellsBlood mononuclear cellsDiabetic foot ulcersM1 macrophage polarizationNovel therapeutic approachesTranscriptomic landscapeWound healing microenvironmentRNA sequencingDFU patientsDevastating complicationFoot ulcerationDFU healingFoot ulcersDFU treatmentMononuclear cellsM1 macrophagesM2 macrophagesMacrophage polarizationTherapeutic approachesSame patientHigh abundance
2020
Effects of short-term physical training on the interleukin-15 signalling pathway and glucose tolerance in aged rats
Minuzzi L, da Conceição L, Muñoz V, Vieira R, Gaspar R, da Silva A, Cintra D, Pereira de Moura L, Ropelle E, Teixeira A, Pauli J. Effects of short-term physical training on the interleukin-15 signalling pathway and glucose tolerance in aged rats. Cytokine 2020, 137: 155306. PMID: 33010727, DOI: 10.1016/j.cyto.2020.155306.Peer-Reviewed Original ResearchMeSH KeywordsAgingAnimalsGlucoseHypoxia-Inducible Factor 1, alpha SubunitHypoxia-Inducible Factor-Proline DioxygenasesInsulin ResistanceInterleukin-15Muscle, SkeletalPhysical Conditioning, AnimalRats, WistarSignal TransductionTime FactorsConceptsAerobic physical trainingInsulin sensitivityIL-15Physical trainingGlucose toleranceInterleukin-15Elderly ratsWhole-body insulin sensitivityShort-term physical trainingSkeletal muscleLast exercise sessionExercise training protocolMesenteric fat massPhysical exercise trainingPhysical exercise protocolSkeletal muscle alterationsFourteen Wistar ratsExpression of HIF1αExercise trainingExercise protocolExercise sessionsMuscle alterationsFat massWistar ratsSupraphysiological levelsNCOA4 is regulated by HIF and mediates mobilization of murine hepatic iron stores after blood loss
Li X, Lozovatsky L, Sukumaran A, Gonzalez L, Jain A, Liu D, Ayala-Lopez N, Finberg KE. NCOA4 is regulated by HIF and mediates mobilization of murine hepatic iron stores after blood loss. Blood 2020, 136: 2691-2702. PMID: 32659785, PMCID: PMC7735158, DOI: 10.1182/blood.2020006321.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBasic Helix-Loop-Helix Transcription FactorsCell LineFemaleGene Expression RegulationGene Knockdown TechniquesHemorrhageHepatocytesHumansHypoxia-Inducible Factor 1, alpha SubunitIronLiverMiceNuclear Receptor CoactivatorsConceptsHepatic iron storesHypoxia-inducible factorNonheme iron concentrationsIron storesBlood lossNCOA4 expressionSubunit levelsHIF-2α knockdownMurine hepatoma cell lineMessenger RNA inductionDietary ironHepatic responseHepatoma cell lineHIF-1αHepatic originIron deficiencyInducible factorMiceCell linesNCOA4PhlebotomyModest effectRNA inductionIron concentrationProlyl hydroxylasesPotent BRD4 inhibitor suppresses cancer cell-macrophage interaction
Yin M, Guo Y, Hu R, Cai WL, Li Y, Pei S, Sun H, Peng C, Li J, Ye R, Yang Q, Wang N, Tao Y, Chen X, Yan Q. Potent BRD4 inhibitor suppresses cancer cell-macrophage interaction. Nature Communications 2020, 11: 1833. PMID: 32286255, PMCID: PMC7156724, DOI: 10.1038/s41467-020-15290-0.Peer-Reviewed Original ResearchMeSH KeywordsAdministration, OralAnimalsCell CommunicationCell Cycle ProteinsCell Line, TumorCell ProliferationDisease Models, AnimalDown-RegulationDrug DesignFemaleHumansHypoxia-Inducible Factor 1, alpha SubunitMacrophage Colony-Stimulating FactorMacrophagesMice, Inbred BALB CMice, NudeNeoplasmsPhosphorylationProto-Oncogene Proteins c-mycReceptors, Granulocyte-Macrophage Colony-Stimulating FactorSignal TransductionTranscription FactorsTreatment OutcomeConceptsTumor growthMajor clinical stagesBET inhibitorsProliferation of tumorsExtraterminal domain (BET) family proteinsTumor cell proliferationClinical stageTumor shrinkageSyngeneic modelPotent BRD4 inhibitorsSmall molecule inhibitorsSolid tumorsBRD4 inhibitionTumor cellsOral bioavailabilityCancer treatmentCell proliferationBRD4 inhibitorsMolecule inhibitorsMultiple mechanismsC-MycTumorsInhibitors
2019
Mechanosensation of cyclical force by PIEZO1 is essential for innate immunity
Solis AG, Bielecki P, Steach HR, Sharma L, Harman CCD, Yun S, de Zoete MR, Warnock JN, To SDF, York AG, Mack M, Schwartz MA, Dela Cruz CS, Palm NW, Jackson R, Flavell RA. Mechanosensation of cyclical force by PIEZO1 is essential for innate immunity. Nature 2019, 573: 69-74. PMID: 31435009, PMCID: PMC6939392, DOI: 10.1038/s41586-019-1485-8.Peer-Reviewed Original ResearchConceptsInnate immune cellsImmune cellsInflammatory responseInnate immune systemCyclical hydrostatic pressurePulmonary inflammationImmune responseImmune systemInnate immunityBacterial infectionsIon channel Piezo1InflammationPhysiological fluctuationsImmunityPhysiological roleLocal microenvironmentCellsPiezo1Direct recognitionResponseAutoinflammationLungInfectionMiceDigoxin improves steatohepatitis with differential involvement of liver cell subsets in mice through inhibition of PKM2 transactivation
Zhao P, Han SN, Arumugam S, Yousaf MN, Qin Y, Jiang JX, Torok NJ, Chen Y, Mankash MS, Liu J, Li J, Iwakiri Y, Ouyang X. Digoxin improves steatohepatitis with differential involvement of liver cell subsets in mice through inhibition of PKM2 transactivation. AJP Gastrointestinal And Liver Physiology 2019, 317: g387-g397. PMID: 31411894, PMCID: PMC6842989, DOI: 10.1152/ajpgi.00054.2019.Peer-Reviewed Original ResearchConceptsHigh-fat dietSignificant clinical applicabilityHuman nonalcoholic steatohepatitisNonalcoholic steatohepatitisOral digoxinLiver injuryCell subsetsPathway activationMouse modelHigh-fat diet mouse modelLiver injury mouse modelHepatocyte mitochondrial dysfunctionClinical applicabilityDiet mouse modelInjury mouse modelDifferential involvementLarge clinical experienceNLRP3 inflammasome activationSignificant protective effectHIF-1α transactivationHepatic oxidative stress responseHypoxia-inducible factorLiver inflammationHFD miceWide dosage rangeCFTR-PTEN–dependent mitochondrial metabolic dysfunction promotes Pseudomonas aeruginosa airway infection
Riquelme SA, Lozano C, Moustafa AM, Liimatta K, Tomlinson KL, Britto C, Khanal S, Gill SK, Narechania A, Azcona-Gutiérrez JM, DiMango E, Saénz Y, Planet P, Prince A. CFTR-PTEN–dependent mitochondrial metabolic dysfunction promotes Pseudomonas aeruginosa airway infection. Science Translational Medicine 2019, 11 PMID: 31270271, PMCID: PMC6784538, DOI: 10.1126/scitranslmed.aav4634.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCarboxy-LyasesColony Count, MicrobialCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorHCT116 CellsHumansHypoxia-Inducible Factor 1, alpha SubunitImmunityInterleukin-1betaLungMice, Inbred C57BLMiddle AgedMitochondriaOxidantsOxidative StressPseudomonas aeruginosaPseudomonas InfectionsPTEN PhosphohydrolaseReactive Oxygen SpeciesSuccinatesConceptsCystic fibrosis transmembrane conductance regulatorImmune-responsive gene 1Fibrosis transmembrane conductance regulatorEffect of PTENTransmembrane conductance regulatorPlasma membraneChromosome 10Reactive oxygen speciesConductance regulatorTumor suppressorTensin homologGene 1Mitochondrial functionMitochondrial activityAnti-inflammatory host responsesCell proliferationOxygen speciesPTENMyeloid cellsCFTR dysfunctionMetabolic defectsHost responseActivity contributesHomologComplexes
2018
SIRT3 deficiency leads to induction of abnormal glycolysis in diabetic kidney with fibrosis
Srivastava SP, Li J, Kitada M, Fujita H, Yamada Y, Goodwin JE, Kanasaki K, Koya D. SIRT3 deficiency leads to induction of abnormal glycolysis in diabetic kidney with fibrosis. Cell Death & Disease 2018, 9: 997. PMID: 30250024, PMCID: PMC6155322, DOI: 10.1038/s41419-018-1057-0.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCarnitine O-PalmitoyltransferaseCell LineDiabetes Mellitus, ExperimentalDiabetic NephropathiesFibrosisGene Knockdown TechniquesGlucoseGlycolysisHumansHypoxia-Inducible Factor 1, alpha SubunitKidneyMiceMice, Inbred C57BLPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPyruvate KinaseSirtuin 3StreptozocinTransfectionTransforming Growth Factor beta2ConceptsDiabetic kidneyAbnormal glycolysisAberrant glycolysisSIRT3 suppressionMouse modelProgressive diabetic kidney diseaseDiabetic kidney diseaseDiabetic mouse modelAberrant glucose metabolismSIRT3 protein levelsSIRT3 siRNADiabetic miceKidney diseaseKidney fibrosisSystemic administrationFibrogenic pathwaysSIRT3 deficiencyGlucose metabolismTherapeutic targetFibrosisSIRT3 levelsHIF1α accumulationFibrogenic phenotypeKidneyGrowth factorCell Autonomous and Non-cell Autonomous Regulation of SMC Progenitors in Pulmonary Hypertension
Sheikh AQ, Saddouk FZ, Ntokou A, Mazurek R, Greif DM. Cell Autonomous and Non-cell Autonomous Regulation of SMC Progenitors in Pulmonary Hypertension. Cell Reports 2018, 23: 1152-1165. PMID: 29694892, PMCID: PMC5959296, DOI: 10.1016/j.celrep.2018.03.043.Peer-Reviewed Original ResearchConceptsPulmonary hypertensionMyeloid cellsPlatelet-derived growth factor receptor βGrowth factor receptor βKruppel-like factor 4Muscle cell markersAttractive therapeutic targetHypoxia-inducible factor-1Vascular muscularizationDistal migrationNormal lungSmall arteriolesMuscle expansionHypertensionTherapeutic targetNon-cell autonomous pathwaysReceptor βCell expressionCell inductionCell markersSMC progenitorsEndothelial cellsFactor 1Factor 4MuscularizationHypoxia-inducible factor 2-alpha-dependent induction of amphiregulin dampens myocardial ischemia-reperfusion injury
Koeppen M, Lee J, Seo S, Brodsky K, Kreth S, Yang I, Buttrick P, Eckle T, Eltzschig H. Hypoxia-inducible factor 2-alpha-dependent induction of amphiregulin dampens myocardial ischemia-reperfusion injury. Nature Communications 2018, 9: 816. PMID: 29483579, PMCID: PMC5827027, DOI: 10.1038/s41467-018-03105-2.Peer-Reviewed Original ResearchMeSH KeywordsAmphiregulinAnimalsBasic Helix-Loop-Helix Transcription FactorsCell LineGene Expression RegulationHumansHypoxia-Inducible Factor 1, alpha SubunitIntegrasesMaleMiceMice, TransgenicMicroarray AnalysisMyocardial Reperfusion InjuryMyocardiumMyocytes, CardiacMyosinsRNA, Small InterferingSignal TransductionConceptsMyocardial ischemia-reperfusion injuryIschemia-reperfusion injuryHypoxia-inducible factorHIF2 alphaCardiac myocytesIschemic heart diseaseGrowth factor amphiregulinMyocardial ischemia toleranceTranscription factor hypoxia-inducible factorHuman cardiac myocytesAreg deficiencyMyocardial inductionElicit cardioprotectionAREG expressionHeart diseaseHIF1 alphaPharmacologic inhibitionIschemia toleranceAmphiregulinCardioprotectionMyocardial tissueInducible deletionMyocytesInjuryMiceDigoxin Suppresses Pyruvate Kinase M2-Promoted HIF-1α Transactivation in Steatohepatitis
Ouyang X, Han SN, Zhang JY, Dioletis E, Nemeth BT, Pacher P, Feng D, Bataller R, Cabezas J, Stärkel P, Caballeria J, Pongratz RL, Cai SY, Schnabl B, Hoque R, Chen Y, Yang WH, Garcia-Martinez I, Wang FS, Gao B, Torok NJ, Kibbey RG, Mehal WZ. Digoxin Suppresses Pyruvate Kinase M2-Promoted HIF-1α Transactivation in Steatohepatitis. Cell Metabolism 2018, 27: 339-350.e3. PMID: 29414684, PMCID: PMC5806149, DOI: 10.1016/j.cmet.2018.01.007.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsCell NucleusChromatinDigoxinDisease Models, AnimalEndotoxinsHistonesHumansHypoxia-Inducible Factor 1, alpha SubunitInflammationLiverNon-alcoholic Fatty Liver DiseaseOxidation-ReductionProtein BindingPyruvate KinaseTHP-1 CellsTranscription, GeneticTranscriptional ActivationConceptsHIF-1α transactivationSterile inflammationHIF-1α pathway activationNon-alcoholic steatohepatitisKinase M2Major clinical consequencesAbility of digoxinLiver inflammationLiver diseasePyruvate kinase M2Clinical consequencesTherapeutic targetInflammationTissue damageHIF-1αPathway activationDigoxinOxidative stressCardiac glycosidesSteatohepatitisDigoxin bindsNovel roleLiverUbiquitous responseActivation
2017
Targeting Hypoxia-Inducible Factor-1α/Pyruvate Dehydrogenase Kinase 1 Axis by Dichloroacetate Suppresses Bleomycin-induced Pulmonary Fibrosis
Goodwin J, Choi H, Hsieh MH, Neugent ML, Ahn JM, Hayenga HN, Singh PK, Shackelford DB, Lee IK, Shulaev V, Dhar S, Takeda N, Kim JW. Targeting Hypoxia-Inducible Factor-1α/Pyruvate Dehydrogenase Kinase 1 Axis by Dichloroacetate Suppresses Bleomycin-induced Pulmonary Fibrosis. American Journal Of Respiratory Cell And Molecular Biology 2017, 58: 216-231. PMID: 28915065, PMCID: PMC5805994, DOI: 10.1165/rcmb.2016-0186oc.Peer-Reviewed Original ResearchConceptsPyruvate dehydrogenase kinase 1Myofibroblast differentiationPulmonary fibrosisFibrotic progressionHIF-1αGlycolytic metabolismDehydrogenase kinase 1Knockout mouse modelHypoxia-inducible factorMetabolic reprogrammingCellular metabolismPotential therapeutic strategyKinase 1Glycolytic switchGenomic deletionsSustained activationMicroenvironmental influencesPreclinical efficacyGlycolytic reprogrammingPharmacological inhibitionReprogrammingMouse modelDifferentiationPharmacological approachesTherapeutic strategiesActivation of NLRP3 inflammasome complex potentiates venous thrombosis in response to hypoxia
Gupta N, Sahu A, Prabhakar A, Chatterjee T, Tyagi T, Kumari B, Khan N, Nair V, Bajaj N, Sharma M, Ashraf MZ. Activation of NLRP3 inflammasome complex potentiates venous thrombosis in response to hypoxia. Proceedings Of The National Academy Of Sciences Of The United States Of America 2017, 114: 4763-4768. PMID: 28420787, PMCID: PMC5422823, DOI: 10.1073/pnas.1620458114.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCaspase 1Disease Models, AnimalFemaleGene Expression RegulationHumansHypoxiaHypoxia-Inducible Factor 1, alpha SubunitInflammasomesInterleukin-1betaMaleNLR Family, Pyrin Domain-Containing 3 ProteinRatsRats, Sprague-DawleyVenous ThrombosisConceptsExpression of NLRP3Venous thrombosisVenous thromboembolismIL-1βCaspase-1Activation of NLRP3Acute thrombotic eventsHypoxic conditionsIL-1β secretionNLRP3 inflammasome complexHypoxia-inducible factorThromboembolic eventsProinflammatory stateSystemic hypoxiaThrombotic eventsPreclinical findingsAltered hemostasisRisk factorsCardiovascular conditionsCommon causeInflammasome activationThrombosisHealthy individualsPyrin domainHIF-1αEndothelial HIF-1α Enables Hypothalamic Glucose Uptake to Drive POMC Neurons
Varela L, Suyama S, Huang Y, Shanabrough M, Tschöp M, Gao XB, Giordano FJ, Horvath TL. Endothelial HIF-1α Enables Hypothalamic Glucose Uptake to Drive POMC Neurons. Diabetes 2017, 66: db161106. PMID: 28292966, PMCID: PMC5440016, DOI: 10.2337/db16-1106.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBehavior, AnimalBlotting, WesternEndotheliumEnergy MetabolismFood DeprivationGene Knockdown TechniquesGlucoseHyperphagiaHypothalamusHypoxia-Inducible Factor 1, alpha SubunitImmunohistochemistryMiceMicroscopy, ElectronMitochondriaNeuronsPatch-Clamp TechniquesPro-OpiomelanocortinReal-Time Polymerase Chain ReactionConceptsPOMC neuronsGlucose uptakePOMC neuronal activityHypothalamic proopiomelanocortin (POMC) neuronsHypoxia-inducible factor-1αProopiomelanocortin neuronsVascular impairmentGlucose administrationMetabolic disordersNeuronal activityMetabolic environmentFactor-1αImpaired functioningEndothelial cellsNeuronsFood deprivationVivoCentral controlHypothalamusMiceAdministrationUptakeImpairmentIncreased Oxidative Stress and Hypoxia Inducible Factor-1 Expression during Arteriovenous Fistula Maturation
Sadaghianloo N, Yamamoto K, Bai H, Tsuneki M, Protack CD, Hall MR, Declemy S, Hassen-Khodja R, Madri J, Dardik A. Increased Oxidative Stress and Hypoxia Inducible Factor-1 Expression during Arteriovenous Fistula Maturation. Annals Of Vascular Surgery 2017, 41: 225-234. PMID: 28163173, PMCID: PMC5411319, DOI: 10.1016/j.avsg.2016.09.014.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAortaArteriovenous Shunt, SurgicalGene Expression RegulationHeme Oxygenase-1Hydrogen PeroxideHyperplasiaHypoxia-Inducible Factor 1, alpha SubunitMaleMembrane ProteinsMice, Inbred C57BLNADPH Oxidase 2NeointimaOxidative StressReactive Oxygen SpeciesSignal TransductionTime FactorsTyrosineVascular Endothelial Growth Factor AVascular PatencyVena Cava, InferiorConceptsHeme oxygenase-1Arteriovenous fistulaAVF maturationNOX-2HIF-1αOxidative stressHypoxia-inducible factor 1 (HIF-1) expressionSham-operated micePoor clinical resultsHIF-1α immunoreactivityInferior vena cavaArteriovenous fistula maturationVascular endothelial growth factorHypoxia-inducible factor-1 (HIF-1) pathwayFactor-1 expressionEndothelial growth factorHIF-1 pathwayHuman AVF maturationQuantitative polymerase chain reactionOxidative stress increasesAortocaval fistulaFistula maturationVena cavaClinical resultsPolymerase chain reactionAmphetamines promote mitochondrial dysfunction and DNA damage in pulmonary hypertension
Chen P, Cao A, Miyagawa K, Tojais N, Hennigs J, Li C, Sweeney N, Inglis A, Wang L, Li D, Ye M, Feldman B, Rabinovitch M. Amphetamines promote mitochondrial dysfunction and DNA damage in pulmonary hypertension. JCI Insight 2017, 2: e90427. PMID: 28138562, PMCID: PMC5256132, DOI: 10.1172/jci.insight.90427.Peer-Reviewed Original ResearchMeSH KeywordsAdultAmphetamine-Related DisordersAmphetaminesAnimalsCaspase 3DNA DamageElectron TransportEndothelial CellsFemaleHumansHypertension, PulmonaryHypoxiaHypoxia-Inducible Factor 1, alpha SubunitIn Vitro TechniquesMaleMethamphetamineMiceMiddle AgedMitochondriaOxidative PhosphorylationProtein Phosphatase 2Protein Serine-Threonine KinasesProto-Oncogene Proteins c-aktPulmonary ArteryPyruvate Dehydrogenase Acetyl-Transferring KinaseReactive Oxygen SpeciesSirtuin 1Vascular RemodelingConceptsPulmonary artery endothelial cellsPulmonary arterial hypertensionDNA damageHypoxic pulmonary artery endothelial cellsDoses of methamphetaminePulmonary vascular remodelingImpaired electron transportActivity of protein phosphatase 2AProtein phosphatase 2AResponse to oxidative stressOxidative stressMitochondrial oxidative phosphorylationArtery endothelial cellsInhibition of AktAdaptive response to oxidative stressMitochondrial ROS increaseBinge dosesDNA damage fociPulmonary hypertensionPyruvate dehydrogenase kinase 1Arterial hypertensionIncreased sirtuin 1Phosphatase 2ATranscriptional activityVascular remodelingThe role of endothelial HIF-1 αin the response to sublethal hypoxia in C57BL/6 mouse pups
Li Q, Michaud M, Park C, Huang Y, Couture R, Girodano F, Schwartz ML, Madri JA. The role of endothelial HIF-1 αin the response to sublethal hypoxia in C57BL/6 mouse pups. Laboratory Investigation 2017, 97: 356-369. PMID: 28092362, DOI: 10.1038/labinvest.2016.154.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornApoptosisBlotting, WesternCell HypoxiaCell ProliferationCells, CulturedDentate GyrusEndothelial CellsFemaleHypoxiaHypoxia-Inducible Factor 1, alpha SubunitLateral VentriclesMaleMice, Inbred C57BLMice, KnockoutMice, TransgenicMicroscopy, FluorescenceMotor ActivityNeural Stem CellsConceptsHIF-1 αBrain microvascular endothelial cellsNeuronal precursor cellsSubventricular zoneMicrovascular endothelial cellsOpen-field activityEndothelial cellsSublethal hypoxiaHIF-1 α expressionOpen-field activity testChronic sublethal hypoxiaEndothelial HIF-1Hypoxic conditionsC57BL/6 mouse pupsGender-specific differencesPremature birthC57BL/6 WTDentate gyrusHippocampal tissueDeficient miceΑ expressionMouse pupsMotor handicapParacrine effectsDentate gyrus tissue
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