Featured Publications
Suppression of angiopoietin-like 4 reprograms endothelial cell metabolism and inhibits angiogenesis
Chaube B, Citrin K, Sahraei M, Singh A, de Urturi D, Ding W, Pierce R, Raaisa R, Cardone R, Kibbey R, Fernández-Hernando C, Suárez Y. Suppression of angiopoietin-like 4 reprograms endothelial cell metabolism and inhibits angiogenesis. Nature Communications 2023, 14: 8251. PMID: 38086791, PMCID: PMC10716292, DOI: 10.1038/s41467-023-43900-0.Peer-Reviewed Original Research
2022
Macrophage-Derived 25-Hydroxycholesterol Promotes Vascular Inflammation, Atherogenesis, and Lesion Remodeling
Canfrán-Duque A, Rotllan N, Zhang X, Andrés-Blasco I, Thompson B, Sun J, Price N, Fernández-Fuertes M, Fowler J, Gómez-Coronado D, Sessa W, Giannarelli C, Schneider R, Tellides G, McDonald J, Fernández-Hernando C, Suárez Y. Macrophage-Derived 25-Hydroxycholesterol Promotes Vascular Inflammation, Atherogenesis, and Lesion Remodeling. Circulation 2022, 147: 388-408. PMID: 36416142, PMCID: PMC9892282, DOI: 10.1161/circulationaha.122.059062.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAtherosclerosisCholesterolHumansHydroxycholesterolsInflammationMacrophagesMiceMice, KnockoutPlaque, AtheroscleroticConceptsLipid-loaded macrophagesLineage-tracing mouse modelsSREBP transcriptional activityCholesterol biosynthetic intermediatesWestern diet feedingAccessible cholesterolDifferent macrophage populationsTranscriptomic analysisKey immune regulatorsPlasma membraneAtherosclerosis progressionImmune activationTranscriptional activityGene expressionDiet feedingInflammatory responseMouse bone marrowLiver X receptorBiosynthetic intermediatesSterol metabolismApoptosis susceptibilityToll-like receptor 4Proinflammatory gene expressionHuman coronary atherosclerotic lesionsMouse atherosclerotic plaquesAntagonism of miR-148a attenuates atherosclerosis progression in APOB TG Apobec -/- Ldlr +/- mice: A brief report
Rotllan N, Zhang X, Canfrán-Duque A, Goedeke L, Griñán R, Ramírez CM, Suárez Y, Fernández-Hernando C. Antagonism of miR-148a attenuates atherosclerosis progression in APOB TG Apobec -/- Ldlr +/- mice: A brief report. Biomedicine & Pharmacotherapy 2022, 153: 113419. PMID: 36076541, PMCID: PMC11140622, DOI: 10.1016/j.biopha.2022.113419.Peer-Reviewed Original ResearchConceptsProgression of atherosclerosisMiR-148aLipoprotein cholesterolAtherosclerotic lesionsHigh-density lipoprotein cholesterolLow-density lipoprotein cholesterolAnti-inflammatory effectsAnti-inflammatory genesMacrophage cholesterol effluxWestern-style dietMiR-148a levelsHepatic gene expressionMurine primary macrophagesAntiatherogenic effectsAtherosclerosis progressionInflammatory responseTherapeutic silencingLipoprotein metabolismPlaque stabilityCholesterol effluxPrimary macrophagesPlaque sizeCholesterol homeostasisLesionsMRNA levels
2021
MMAB promotes negative feedback control of cholesterol homeostasis
Goedeke L, Canfrán-Duque A, Rotllan N, Chaube B, Thompson BM, Lee RG, Cline GW, McDonald JG, Shulman GI, Lasunción MA, Suárez Y, Fernández-Hernando C. MMAB promotes negative feedback control of cholesterol homeostasis. Nature Communications 2021, 12: 6448. PMID: 34750386, PMCID: PMC8575900, DOI: 10.1038/s41467-021-26787-7.Peer-Reviewed Original ResearchMeSH KeywordsAlkyl and Aryl TransferasesAnimalsCell Line, TumorCholesterolCholesterol, LDLFeedback, PhysiologicalGene Expression ProfilingHeLa CellsHep G2 CellsHomeostasisHumansHydroxymethylglutaryl CoA ReductasesLiverMice, Inbred C57BLMice, KnockoutPromoter Regions, GeneticReceptors, LDLRNA InterferenceSterol Regulatory Element Binding Protein 2ConceptsCholesterol biosynthesisCholesterol homeostasisMouse hepatic cell lineIntegrative genomic strategyIntricate regulatory networkMaster transcriptional regulatorCellular cholesterol levelsHMGCR activityLDL-cholesterol uptakeCholesterol levelsHuman hepatic cellsSterol contentGenomic strategiesTranscriptional regulatorsRegulatory networksIntracellular cholesterol levelsGene expressionUnexpected roleHepatic cell linesBiosynthesisMMABIntracellular levelsCell linesHomeostasisExpression of SREBP2
2020
Cav-1 (Caveolin-1) Deficiency Increases Autophagy in the Endothelium and Attenuates Vascular Inflammation and Atherosclerosis
Zhang X, Ramírez CM, Aryal B, Madrigal-Matute J, Liu X, Diaz A, Torrecilla-Parra M, Suárez Y, Cuervo AM, Sessa WC, Fernández-Hernando C. Cav-1 (Caveolin-1) Deficiency Increases Autophagy in the Endothelium and Attenuates Vascular Inflammation and Atherosclerosis. Arteriosclerosis Thrombosis And Vascular Biology 2020, 40: 1510-1522. PMID: 32349535, PMCID: PMC7253189, DOI: 10.1161/atvbaha.120.314291.Peer-Reviewed Original ResearchConceptsCav-1 deficiencyCav-1-deficient miceCav-1Autophagic fluxCholesterol-rich membrane domainsCav-1 interactsATG5-ATG12 complexEndothelial Cav-1 expressionRegulation of autophagyNovel molecular mechanismExtracellular matrix remodelingAutophagosome componentsMembrane domainsLipid raftsAutophagosome formationPlasma membraneCav-1 expressionMolecular mechanismsLDL transcytosisCellular localizationImportant regulatorAutophagyAutophagy contributesRelevant regulatorMatrix remodeling
2019
Genetic deficiency or pharmacological inhibition of miR-33 protects from kidney fibrosis
Price NL, Miguel V, Ding W, Singh AK, Malik S, Rotllan N, Moshnikova A, Toczek J, Zeiss C, Sadeghi MM, Arias N, Baldán Á, Andreev OA, Rodríguez-Puyol D, Bahal R, Reshetnyak YK, Suárez Y, Fernández-Hernando C, Lamas S. Genetic deficiency or pharmacological inhibition of miR-33 protects from kidney fibrosis. JCI Insight 2019, 4 PMID: 31613798, PMCID: PMC6948871, DOI: 10.1172/jci.insight.131102.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsFatty AcidsFibrosisKidney DiseasesMaleMiceMice, Inbred C57BLMice, KnockoutMicroRNAsOxidation-ReductionConceptsFatty acid oxidationChronic kidney diseaseKidney diseaseDisease progressionMiR-33Bone marrow transplantExtent of fibrosisDevelopment of fibrosisAttractive therapeutic targetExpression of factorsNucleic acid inhibitorsMarrow transplantKidney fibrosisFibrotic kidneysMouse modelTherapeutic targetLipid metabolismPharmacological inhibitionFibrosisLipid accumulationDiseaseGenetic deficiencyProgressionKidneyAcid oxidationCaveolin-1 Regulates Atherogenesis by Attenuating Low-Density Lipoprotein Transcytosis and Vascular Inflammation Independently of Endothelial Nitric Oxide Synthase Activation
Ramírez CM, Zhang X, Bandyopadhyay C, Rotllan N, Sugiyama MG, Aryal B, Liu X, He S, Kraehling JR, Ulrich V, Lin CS, Velazquez H, Lasunción MA, Li G, Suárez Y, Tellides G, Swirski FK, Lee WL, Schwartz MA, Sessa WC, Fernández-Hernando C. Caveolin-1 Regulates Atherogenesis by Attenuating Low-Density Lipoprotein Transcytosis and Vascular Inflammation Independently of Endothelial Nitric Oxide Synthase Activation. Circulation 2019, 140: 225-239. PMID: 31154825, PMCID: PMC6778687, DOI: 10.1161/circulationaha.118.038571.Peer-Reviewed Original ResearchConceptsEndothelial nitric oxide synthaseDiet-induced atherosclerosisNO productionVascular inflammationENOS activationEndothelial nitric oxide synthase activationNitric oxide synthase activationAthero-protective functionsLipid metabolic factorsEndothelial cell inflammationNitric oxide synthaseWild-type miceMice Lacking ExpressionProduction of NOExtracellular matrix remodelingInflammatory primingHyperlipidemic miceInflammatory pathwaysAortic archCell inflammationOxide synthaseMetabolic factorsMouse modelAtherosclerosisInflammationSpecific Disruption of Abca1 Targeting Largely Mimics the Effects of miR-33 Knockout on Macrophage Cholesterol Efflux and Atherosclerotic Plaque Development
Price NL, Rotllan N, Zhang X, Canfrán-Duque A, Nottoli T, Suarez Y, Fernández-Hernando C. Specific Disruption of Abca1 Targeting Largely Mimics the Effects of miR-33 Knockout on Macrophage Cholesterol Efflux and Atherosclerotic Plaque Development. Circulation Research 2019, 124: 874-880. PMID: 30707082, PMCID: PMC6417928, DOI: 10.1161/circresaha.118.314415.Peer-Reviewed Original ResearchConceptsMacrophage cholesterol effluxAtherosclerotic plaque formationCholesterol effluxMiR-33Proatherogenic effectsABCA1 expressionBone marrowDeficient animalsPlaque formationMiR-33-deficient miceHigh-fat diet feedingHepatic ABCA1 expressionAtherosclerotic plaque burdenFat diet feedingDevelopment of obesityNovel mouse modelAtherosclerotic plaque developmentFoam cell formationPlaque burdenDeficient miceDiet feedingMetabolic dysfunctionSpecific disruptionMouse modelKnockout mice
2018
Absence of ANGPTL4 in adipose tissue improves glucose tolerance and attenuates atherogenesis
Aryal B, Singh AK, Zhang X, Varela L, Rotllan N, Goedeke L, Chaube B, Camporez JP, Vatner DF, Horvath TL, Shulman GI, Suárez Y, Fernández-Hernando C. Absence of ANGPTL4 in adipose tissue improves glucose tolerance and attenuates atherogenesis. JCI Insight 2018, 3: e97918. PMID: 29563332, PMCID: PMC5926923, DOI: 10.1172/jci.insight.97918.Peer-Reviewed Original ResearchMeSH KeywordsAdipocytesAdipose TissueAllelesAngiopoietin-Like Protein 4AnimalsAtherosclerosisBody WeightChemokinesCytokinesDiet, High-FatDiet, WesternFatty AcidsGene Expression ProfilingGene Expression RegulationGene Knockout TechniquesGlucoseInsulinIntegrasesIntercellular Signaling Peptides and ProteinsLipid MetabolismLipoprotein LipaseLipoproteinsLiverMaleMiceMice, Inbred C57BLMice, KnockoutMusclesObesityProprotein Convertase 9TriglyceridesConceptsAngiopoietin-like protein 4High-fat dietEctopic lipid depositionLipid depositionGlucose toleranceLipoprotein lipaseShort-term high-fat dietSevere metabolic abnormalitiesProgression of atherosclerosisMajor risk factorTriacylglycerol-rich lipoproteinsFatty acid uptakeAdipose tissue resultsProatherogenic lipoproteinsCardiometabolic diseasesMetabolic abnormalitiesKO miceRisk factorsWhole body lipidMetabolic disordersGlucose metabolismLPL activityAdipose tissueGenetic ablationRapid clearance
2017
Genetic Dissection of the Impact of miR-33a and miR-33b during the Progression of Atherosclerosis
Price NL, Rotllan N, Canfrán-Duque A, Zhang X, Pati P, Arias N, Moen J, Mayr M, Ford DA, Baldán Á, Suárez Y, Fernández-Hernando C. Genetic Dissection of the Impact of miR-33a and miR-33b during the Progression of Atherosclerosis. Cell Reports 2017, 21: 1317-1330. PMID: 29091769, PMCID: PMC5687841, DOI: 10.1016/j.celrep.2017.10.023.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAortaAtherosclerosisATP Binding Cassette Transporter 1Blood GlucoseCells, CulturedCholesterolCholesterol, HDLDisease ProgressionGene Regulatory NetworksMacrophages, PeritonealMaleMiceMice, Inbred C57BLMice, KnockoutMicroRNAsMitochondrial Trifunctional Protein, beta SubunitMyocardiumReceptors, LDLConceptsPlaque burdenMiR-33MiR-33-deficient miceReduced plaque burdenProgression of atherosclerosisPro-atherogenic effectsMacrophage cholesterol effluxDecreases lipid accumulationTreatment of atherosclerosisMacrophage-specific lossMiR-33 deficiencyPromotes obesityHDL levelsInsulin resistancePlaque macrophagesProtective effectHyperlipidemic conditionsCholesterol effluxPlaque developmentLipid metabolismAtherosclerosisLipid accumulationHDL biogenesisPromising targetMacrophagesMacrophage deficiency of miR‐21 promotes apoptosis, plaque necrosis, and vascular inflammation during atherogenesis
Canfrán‐Duque A, Rotllan N, Zhang X, Fernández‐Fuertes M, Ramírez‐Hidalgo C, Araldi E, Daimiel L, Busto R, Fernández‐Hernando C, Suárez Y. Macrophage deficiency of miR‐21 promotes apoptosis, plaque necrosis, and vascular inflammation during atherogenesis. EMBO Molecular Medicine 2017, 9: 1244-1262. PMID: 28674080, PMCID: PMC5582411, DOI: 10.15252/emmm.201607492.Peer-Reviewed Original ResearchConceptsER stress-induced apoptosisPost-translational degradationFoam cell formationMiR-21MiR-21 target genesTarget genesJNK signalingPlaque necrosisAbundant miRNAVascular inflammationAccumulation of lipidsHematopoietic cellsMacrophage apoptosisCell formationAberrant expressionMacrophage deficiencyApoptosisCholesterol effluxProgression of atherosclerosisChronic inflammatory diseasePathophysiological processesInflammatory cellsExpressionInflammatory diseasesCardiovascular disease
2015
VEGF-Induced Expression of miR-17–92 Cluster in Endothelial Cells Is Mediated by ERK/ELK1 Activation and Regulates Angiogenesis
Chamorro-Jorganes A, Lee MY, Araldi E, Landskroner-Eiger S, Fernández-Fuertes M, Sahraei M, del Rey M, van Solingen C, Yu J, Fernández-Hernando C, Sessa WC, Suárez Y. VEGF-Induced Expression of miR-17–92 Cluster in Endothelial Cells Is Mediated by ERK/ELK1 Activation and Regulates Angiogenesis. Circulation Research 2015, 118: 38-47. PMID: 26472816, PMCID: PMC4703066, DOI: 10.1161/circresaha.115.307408.Peer-Reviewed Original ResearchConceptsMiR-17Elk1 activationEndothelial angiogenic functionEC proliferationRegulation of angiogenesisTranscription activationTranscriptional programsGenetic evidenceCluster expressionTumor angiogenesisAngiogenic sproutingVEGF stimulationRescue experimentsRetinal angiogenesisRegulate angiogenesisLines of evidenceEndothelial cell functionAngiogenic switchPhysiological retinal angiogenesisAngiogenic functionDevelopmental retinal angiogenesisCell functionTumor developmentRegulationCrucial mediator
2014
Hematopoietic Akt2 deficiency attenuates the progression of atherosclerosis
Rodlan N, Chamorro‐Jorganes A, Araldi E, Wanschel AC, Aryal B, Aranda JF, Goedeke L, Salerno AG, Ramírez CM, Sessa WC, Suárez Y, Fernández‐Hernando C. Hematopoietic Akt2 deficiency attenuates the progression of atherosclerosis. The FASEB Journal 2014, 29: 597-610. PMID: 25392271, PMCID: PMC4314230, DOI: 10.1096/fj.14-262097.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAtherosclerosisBlood GlucoseBone Marrow CellsBone Marrow TransplantationCell MovementCholesterolCytokinesDisease ProgressionInflammationInsulinLeukocytesLipidsLipoproteins, LDLMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutMicroscopy, ConfocalMicroscopy, FluorescencePlaque, AtheroscleroticProto-Oncogene Proteins c-aktReceptors, LDLConceptsProgression of atherosclerosisSerine-threonine protein kinaseBone marrow cellsAkt2-deficient miceInsulin-responsive tissuesWild-type bone marrow cellsProtein kinaseMarrow cellsAkt2 deficiencyAkt2Higher plasma lipidsWild-type miceMice resultsProatherogenic cytokinesObese subjectsPlasma lipidsProinflammatory cytokinesInsulin resistanceInflammatory responseGlucose levelsAtherosclerotic plaquesCholesterol metabolismAtherosclerosisMacrophage migrationMarked reductionImproved repair of dermal wounds in mice lacking microRNA‐155
van Solingen C, Araldi E, Chamorro‐Jorganes A, Fernández‐Hernando C, Suárez Y. Improved repair of dermal wounds in mice lacking microRNA‐155. Journal Of Cellular And Molecular Medicine 2014, 18: 1104-1112. PMID: 24636235, PMCID: PMC4112003, DOI: 10.1111/jcmm.12255.Peer-Reviewed Original ResearchConceptsMiR-155Wound tissueWound healingIncreased expressionWound closureImpaired wound repairAnalysis of woundsSkin of miceMiR-155 targetsType 1 collagenWild-type animalsInflammatory mediatorsWT miceWound healing processImmune responseInterleukin-4Healthy skinMicroRNA-155Punch woundsMiceElevated numbersBeneficial effectsWound closingDermal wound healingDermal wounds
2013
Control of Cholesterol Metabolism and Plasma High-Density Lipoprotein Levels by microRNA-144
Ramírez CM, Rotllan N, Vlassov AV, Dávalos A, Li M, Goedeke L, Aranda JF, Cirera-Salinas D, Araldi E, Salerno A, Wanschel A, Zavadil J, Castrillo A, Kim J, Suárez Y, Fernández-Hernando C. Control of Cholesterol Metabolism and Plasma High-Density Lipoprotein Levels by microRNA-144. Circulation Research 2013, 112: 1592-1601. PMID: 23519695, PMCID: PMC3929583, DOI: 10.1161/circresaha.112.300626.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnticholesteremic AgentsApolipoprotein A-IATP Binding Cassette Transporter 1ATP-Binding Cassette TransportersChlorocebus aethiopsCholesterol, HDLCOS CellsDiet, High-FatGene Expression ProfilingHep G2 CellsHepatocytesHomeostasisHumansHydrocarbons, FluorinatedLiver X ReceptorsMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutMicroRNAsOligonucleotide Array Sequence AnalysisOligonucleotidesOrphan Nuclear ReceptorsSulfonamidesConceptsAdenosine triphosphate-binding cassette transporter A1Liver X nuclear receptorCholesterol metabolismABCA1 expressionMiR-144HDL levelsLXR agonistsCholesterol effluxLXR ligandsHigh-density lipoprotein levelsPlasma high-density lipoprotein levelsTriphosphate-binding cassette transporter A1Potential therapeutical interventionsAtherosclerotic vascular diseaseMacrophage cholesterol effluxCassette transporter A1Cassette transporter G1MiR-144 expressionPrimary mouse peritoneal macrophagesHigh-density lipoprotein biogenesisEfflux of cholesterolFoam cell formationAdenosine triphosphate-binding cassette transportersModulation of miRNAsMiRNA expression signatures
2011
Antagonism of miR-33 in mice promotes reverse cholesterol transport and regression of atherosclerosis
Rayner KJ, Sheedy FJ, Esau CC, Hussain FN, Temel RE, Parathath S, van Gils JM, Rayner AJ, Chang AN, Suarez Y, Fernandez-Hernando C, Fisher EA, Moore KJ. Antagonism of miR-33 in mice promotes reverse cholesterol transport and regression of atherosclerosis. Journal Of Clinical Investigation 2011, 121: 2921-2931. PMID: 21646721, PMCID: PMC3223840, DOI: 10.1172/jci57275.Peer-Reviewed Original ResearchConceptsABC transporter A1HDL levelsRegression of atherosclerosisCholesterol transportMiR-33MiR-33 inhibitionAtherosclerotic vascular diseasePlasma HDL levelsInflammatory gene expressionReverse cholesterol transportABCA1 levelsAtherosclerosis regressionVascular diseasePlaque macrophagesPlaque stabilityABCA1 expressionAtherosclerotic plaquesMice promotesProtective roleLipid metabolismLDL receptorClinical therapyPlaque sizeAtherosclerosisSREBF2 gene
2010
MicroRNAs Are Necessary for Vascular Smooth Muscle Growth, Differentiation, and Function
Albinsson S, Suarez Y, Skoura A, Offermanns S, Miano JM, Sessa WC. MicroRNAs Are Necessary for Vascular Smooth Muscle Growth, Differentiation, and Function. Arteriosclerosis Thrombosis And Vascular Biology 2010, 30: 1118-1126. PMID: 20378849, PMCID: PMC2880481, DOI: 10.1161/atvbaha.109.200873.Peer-Reviewed Original ResearchMeSH KeywordsActinsAnimalsAortaCell DifferentiationCell ProliferationCells, CulturedDEAD-box RNA HelicasesEmbryo LossEndoribonucleasesGene Expression Regulation, DevelopmentalGenotypeGestational AgeHemorrhageIntegrasesLiver DiseasesMaleMiceMice, KnockoutMicrofilament ProteinsMicroRNAsMuscle DevelopmentMuscle ProteinsMuscle, Smooth, VascularNuclear ProteinsPhenotypeRibonuclease IIIStress FibersTrans-ActivatorsTranscriptional ActivationTransfectionUmbilical ArteriesVasoconstrictionVasodilationConceptsLate embryonic lethalityFundamental cellular processesContractile differentiationContractile protein markersDicer-dependent miRNAsActin stress fibersDeletion of DicerRole of miRNAsDicer resultsOverexpression of microRNAEmbryonic lethalityMiRNA synthesisCellular processesRate-limiting enzymeStress fibersVascular developmentMuscle growthCell typesCellular proliferationMiRNAsVascular smooth muscle growthVascular smooth muscle proliferationMicroRNAsProtein markersDicer
2009
Reticulon 4B (Nogo-B) is necessary for macrophage infiltration and tissue repair
Yu J, Fernández-Hernando C, Suarez Y, Schleicher M, Hao Z, Wright PL, DiLorenzo A, Kyriakides TR, Sessa WC. Reticulon 4B (Nogo-B) is necessary for macrophage infiltration and tissue repair. Proceedings Of The National Academy Of Sciences Of The United States Of America 2009, 106: 17511-17516. PMID: 19805174, PMCID: PMC2762666, DOI: 10.1073/pnas.0907359106.Peer-Reviewed Original ResearchConceptsBlood vessel assemblyBone marrow-derived macrophagesBone marrow reconstitution experimentsMarrow-derived macrophagesRac activationBlood vessel formationGene expressionReconstitution experimentsMacrophage infiltrationInflammatory gene expressionVessel formationBlood flow recoveryMacrophage-mediated inflammationTissue repairMyeloid cellsBlood flow controlVessel assemblyLimb ischemiaFunctional recoveryInflammatory responseReticulon 4BWound healingIschemiaFlow recoveryGenesGenetic Evidence Supporting a Critical Role of Endothelial Caveolin-1 during the Progression of Atherosclerosis
Fernández-Hernando C, Yu J, Suárez Y, Rahner C, Dávalos A, Lasunción MA, Sessa WC. Genetic Evidence Supporting a Critical Role of Endothelial Caveolin-1 during the Progression of Atherosclerosis. Cell Metabolism 2009, 10: 48-54. PMID: 19583953, PMCID: PMC2735117, DOI: 10.1016/j.cmet.2009.06.003.Peer-Reviewed Original ResearchConceptsProgression of atherosclerosisInitiation of atherosclerosisCav-1ApoE knockout backgroundArtery wallKnockout backgroundLeukocyte adhesion moleculesNitric oxide productionEndothelial Cav-1 expressionCav-1 expressionEndothelial caveolin-1AtherosclerosisTransgenic miceOxide productionGenetic ablationLDL infiltrationAdhesion moleculesCritical roleCaveolin-1 geneLDL-derived cholesterolMiceVessel wallPhysiological evidenceLesion expansionGenetic evidence
2007
Loss of Akt1 Leads to Severe Atherosclerosis and Occlusive Coronary Artery Disease
Fernández-Hernando C, Ackah E, Yu J, Suárez Y, Murata T, Iwakiri Y, Prendergast J, Miao RQ, Birnbaum MJ, Sessa WC. Loss of Akt1 Leads to Severe Atherosclerosis and Occlusive Coronary Artery Disease. Cell Metabolism 2007, 6: 446-457. PMID: 18054314, PMCID: PMC3621848, DOI: 10.1016/j.cmet.2007.10.007.Peer-Reviewed Original ResearchMeSH KeywordsAcute Coronary SyndromeAnimalsApolipoproteins EApoptosisAtherosclerosisBone Marrow TransplantationCoronary OcclusionDisease Models, AnimalEndothelial CellsFemaleHumansInflammation MediatorsMacrophagesMaleMiceMice, KnockoutNitric Oxide Synthase Type IINitric Oxide Synthase Type IIIProto-Oncogene Proteins c-aktConceptsLoss of Akt1Apolipoprotein E knockout backgroundOcclusive coronary artery diseaseBone marrow transfer experimentsAcute coronary syndromeCoronary artery diseaseLesion expansionCoronary syndromeCoronary atherosclerosisSevere atherosclerosisArtery diseaseInflammatory mediatorsCoronary lesionsVascular protectionVascular originProinflammatory genesENOS phosphorylationCardiovascular systemLesion formationGenetic ablationEndothelial cellsAtherogenesisEnhanced expressionKnockout backgroundVessel wall