2023
Evidence Accumulates: Patients with Ascending Aneurysms Are Strongly Protected from Atherosclerotic Disease
Waldron C, Zafar M, Ziganshin B, Weininger G, Grewal N, Elefteriades J. Evidence Accumulates: Patients with Ascending Aneurysms Are Strongly Protected from Atherosclerotic Disease. International Journal Of Molecular Sciences 2023, 24: 15640. PMID: 37958625, PMCID: PMC10650782, DOI: 10.3390/ijms242115640.Peer-Reviewed Original ResearchConceptsThoracic aortic aneurysmAortic aneurysmCarotid intima-media thicknessLow-density lipoprotein levelsIntima-media thicknessDevelopment of atherosclerosisMatrix metalloproteinase proteinsAscending aneurysmAortic calcificationAtherosclerotic diseaseLipoprotein levelsMyocardial infarctionLeading causeAneurysmsMetalloproteinase proteinsGrowth factorProtective relationshipDiseasePossible mechanismCurrent understandingMorbidityInfarctionAtherosclerosisPatientsPathophysiologyCase report: Coronary atherosclerosis in a patient with long-standing very low LDL-C without lipid-lowering therapy
Mottola G, Welty F, Mojibian H, Faridi K. Case report: Coronary atherosclerosis in a patient with long-standing very low LDL-C without lipid-lowering therapy. Frontiers In Cardiovascular Medicine 2023, 10: 1272944. PMID: 37795488, PMCID: PMC10546007, DOI: 10.3389/fcvm.2023.1272944.Peer-Reviewed Case Reports and Technical NotesLipid-Lowering TherapyLDL-C levelsCoronary atherosclerosisLow LDL-C levelsLow-density lipoprotein cholesterolCardiovascular risk factorsLeft coronary systemRight coronary arteryLow serum levelsDevelopment of atherosclerosisNonobstructive coronary atherosclerosisRoutine laboratory dataTomography angiography scansApoB-containing lipoproteinsHeterozygous familial hypobetalipoproteinemiaAnomalous originMyxoma resectionAcute strokeAtrial myxomaCardiovascular riskLipoprotein cholesterolPlaque regressionDiabetes mellitusPrimordial preventionSerum levels
2022
Endometriosis promotes atherosclerosis in a murine model
Mamillapalli R, Toffoloni N, Habata S, Qunhua H, Atwani R, Stachenfeld N, Taylor HS. Endometriosis promotes atherosclerosis in a murine model. American Journal Of Obstetrics And Gynecology 2022, 227: 248.e1-248.e8. PMID: 35351413, PMCID: PMC9308711, DOI: 10.1016/j.ajog.2022.03.040.Peer-Reviewed Original ResearchConceptsEffect of endometriosisOil Red O stainingVascular endothelial growth factorMurine modelCardiovascular diseaseRed O stainingEndothelial growth factorSham miceEndometriotic lesionsInflammatory cytokinesInterleukin-6Luminal areaInterferon gammaO stainingGrowth factorAortic luminal areasInflammatory-related cytokinesRoot wall thicknessUnderwent sham surgeryTreatment of endometriosisInflammation-related cytokinesDevelopment of atherosclerosisApolipoprotein E (ApoE<sup>-/-</sup>) miceLong-term riskWeeks of induction
2020
Uncovering the Specific Functions of miR-33 in Regulation of Feeding and Cardiometabolic Diseases Linked to Aging
Price N, Zhang X, Fernandez-Tussy P, de Cabo R, Fernandez-Hernando C. Uncovering the Specific Functions of miR-33 in Regulation of Feeding and Cardiometabolic Diseases Linked to Aging. Innovation In Aging 2020, 4: 128-128. PMCID: PMC7741365, DOI: 10.1093/geroni/igaa057.421.Peer-Reviewed Original ResearchMiR-33Cardiometabolic diseasesMetabolic dysfunctionHigh fat diet fed miceFat Diet-Fed MiceMetabolic tissuesDiet fed miceDevelopment of obesityMacrophage cholesterol effluxDevelopment of atherosclerosisRegulation of feedingCholesterol transporter ABCA1Unique mouse modelKey metabolic tissuesDifferent metabolic tissuesFeeding behaviorFed miceHeart diseaseInflammatory responseMouse modelRelated health issuesCholesterol effluxKnockout miceDeficient animalsAtherosclerosis
2019
ARHGAP18: A Flow‐Responsive Gene That Regulates Endothelial Cell Alignment and Protects Against Atherosclerosis
Lay AJ, Coleman PR, Formaz‐Preston A, Ting KK, Roediger B, Weninger W, Schwartz MA, Vadas MA, Gamble JR. ARHGAP18: A Flow‐Responsive Gene That Regulates Endothelial Cell Alignment and Protects Against Atherosclerosis. Journal Of The American Heart Association 2019, 8: e010057. PMID: 30630384, PMCID: PMC6497359, DOI: 10.1161/jaha.118.010057.Peer-Reviewed Original ResearchConceptsApolipoprotein EHigh-fat diet-induced modelIntercellular adhesion molecule-1Endothelial nitric oxide synthaseHigh-fat dietDevelopment of atherosclerosisNitric oxide synthaseDiet-induced modelAdhesion molecule-1Double mutant miceAortic diseaseAtherosclerosis developmentInflammatory phenotypeOxide synthaseMolecule-1AtherosclerosisEarly onsetProtective genesMiceFlow-responsive genesAtheroprotective regionsEndothelial cell alignmentAdaptive responseAnalysis of ECEC ability
2018
Non-coding RNA regulation of endothelial and macrophage functions during atherosclerosis
Aryal B, Suárez Y. Non-coding RNA regulation of endothelial and macrophage functions during atherosclerosis. Vascular Pharmacology 2018, 114: 64-75. PMID: 29551552, PMCID: PMC6177333, DOI: 10.1016/j.vph.2018.03.001.Peer-Reviewed Original ResearchConceptsNon-coding RNAsNon-coding RNA regulationSmall non-coding RNAsMultiple cell functionsRNA regulationMacrophage functionRNA moleculesGene expressionPotential regulatorKey playersVascular biologyPathogenesis of atherosclerosisCell functionSpecific roleLncRNAsRegulationRNAMechanism of actionEndothelial cellsInitial eventVascular integrityRecruitment of monocytesMicroRNAsDevelopment of atherosclerosisBiology
2016
Down-regulation of Insulin Receptor Substrate 1 during Hyperglycemia Induces Vascular Smooth Muscle Cell Dedifferentiation*
Xi G, Wai C, White M, Clemmons D. Down-regulation of Insulin Receptor Substrate 1 during Hyperglycemia Induces Vascular Smooth Muscle Cell Dedifferentiation*. Journal Of Biological Chemistry 2016, 292: 2009-2020. PMID: 28003360, PMCID: PMC5290970, DOI: 10.1074/jbc.m116.758987.Peer-Reviewed Original ResearchConceptsInsulin receptor substrate-1Receptor substrate-1IRS-1Differentiated stateSubstrate-1Aberrant signalingMetabolic stressVascular smooth muscle cell dedifferentiationIGF-I stimulationIRS-1 expressionVascular smooth muscle cell migrationScaffold proteinSHPS-1Transcription factorsSmooth muscle cell dedifferentiationSmooth muscle cell migrationMuscle cell dedifferentiationMuscle cell migrationReceptor signalsVSMC dedifferentiationCell migrationInsulin-like growth factor ICell dedifferentiationMajor risk factorDevelopment of atherosclerosisSystemic and cell-specific mechanisms of vasculopathy induced by human immunodeficiency virus and highly active antiretroviral therapy
Haser GC, Sumpio B. Systemic and cell-specific mechanisms of vasculopathy induced by human immunodeficiency virus and highly active antiretroviral therapy. Journal Of Vascular Surgery 2016, 65: 849-859. PMID: 26994951, DOI: 10.1016/j.jvs.2016.01.036.Peer-Reviewed Original ResearchConceptsHuman immunodeficiency virusActive antiretroviral therapySmooth muscle cellsAntiretroviral therapyHIV patientsImmunodeficiency virusTraditional cardiovascular risk factorsMuscle cellsEndothelial cellsCardiovascular risk factorsChronic immune activationSerious cardiovascular eventsDevelopment of atherosclerosisVascular systemCardiovascular eventsVascular complicationsHIV medicationsChronic inflammationImmune activationMyocardial infarctionRisk factorsCell-specific mechanismsGeneral populationCholesterol metabolismCardiovascular pathology
2015
The role of microRNAs in coronary artery disease: From pathophysiology to diagnosis and treatment
Economou EK, Oikonomou E, Siasos G, Papageorgiou N, Tsalamandris S, Mourouzis K, Papaioanou S, Tousoulis D. The role of microRNAs in coronary artery disease: From pathophysiology to diagnosis and treatment. Atherosclerosis 2015, 241: 624-633. PMID: 26117399, DOI: 10.1016/j.atherosclerosis.2015.06.037.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsMeSH KeywordsAnimalsApoptosisAtherosclerosisBiomarkersBlood PlateletsCell MovementCoronary Artery DiseaseDisease ProgressionEndothelium, VascularGene Expression RegulationHumansLipoproteins, HDLLipoproteins, LDLMiceMicroRNAsMonocytesMuscle, Smooth, VascularMyocardial InfarctionNeovascularization, PathologicOligonucleotidesReperfusion InjuryStem CellsConceptsCoronary artery diseaseDevelopment of atherosclerosisArtery diseaseCoronary artery disease progressionPathogenesis of atherosclerosisStudy of miRNAsMyocardial infarctionDisease progressionSpecific miRNA expression patternsTherapeutic approachesRole of microRNAsPreventive opportunitiesDiagnostic biomarkersRelated conditionsAtherosclerosisMiRNA expression patternsDiseaseNon-coding RNA moleculesRole of miRNAsIntercellular communicationIntracellular regulatorsExpression patternsMiRNAsPost-transcriptional levelGene expression
2013
Deletion of angiotensin-converting enzyme 2 promotes the development of atherosclerosis and arterial neointima formation
Sahara M, Ikutomi M, Morita T, Minami Y, Nakajima T, Hirata Y, Nagai R, Sata M. Deletion of angiotensin-converting enzyme 2 promotes the development of atherosclerosis and arterial neointima formation. Cardiovascular Research 2013, 101: 236-246. PMID: 24193738, DOI: 10.1093/cvr/cvt245.Peer-Reviewed Original ResearchMeSH KeywordsAngiotensin IIAngiotensin-Converting Enzyme 2AnimalsAortaAortic DiseasesApolipoproteins EAtherosclerosisCell ProliferationCells, CulturedDisease Models, AnimalFemoral ArteryGene DeletionGenetic Predisposition to DiseaseInflammation MediatorsJNK Mitogen-Activated Protein KinasesMacrophagesMiceMice, Inbred C57BLMice, KnockoutMuscle, Smooth, VascularMyocytes, Smooth MuscleNeointimaPeptidyl-Dipeptidase APhenotypePlaque, AtheroscleroticProtein Kinase InhibitorsRNA InterferenceSignal TransductionTransfectionVascular System InjuriesConceptsVascular smooth muscle cellsAortic vascular smooth muscle cellsArterial neointima formationVascular diseaseACE2 deficiencyVascular lesionsEnzyme 2Neointima formationApolipoprotein E knockout miceVascular cell adhesion moleculeACE2 KO miceLarge vascular lesionsAngiotensin II levelsRenin-angiotensin systemE knockout miceAortic atherosclerotic plaquesPro-inflammatory phenotypeRole of ACE2Development of atherosclerosisInflammation-related genesArterial neointimal hyperplasiaTumor necrosis factorSmooth muscle cellsPrimary bone marrow macrophagesDeletion of angiotensinOsteoprotegerin and osteopontin serum levels are associated with vascular function and inflammatory process in coronary artery disease
Maniatis K, Siasos G, Tousoulis D, Oikonomou E, Zaromitidou M, Kioufis S, Kokkou E, Gouliopoulos N, Mazaris S, Stefanadis C. Osteoprotegerin and osteopontin serum levels are associated with vascular function and inflammatory process in coronary artery disease. European Heart Journal 2013, 34: p606. DOI: 10.1093/eurheartj/eht307.p606.Peer-Reviewed Original ResearchCoronary artery diseasePulse wave velocityInterleukin-6 serum levelsInterleukin-6 levelsCAD patientsSerum levelsOPN serum levelsEndothelial functionVascular functionArtery diseaseArterial stiffnessOPG levelsControl subjectsCarotid-femoral pulse wave velocityOPG serum levelsOsteopontin serum levelsRelation of OsteoprotegerinSerum OPG levelsAdverse cardiovascular outcomesDevelopment of atherosclerosisLarge population studiesArterial wall stiffeningCardiovascular outcomesInflammatory markersAortic stiffness
2012
Carotid Intima-Media Thickness Provides Evidence that Ascending Aortic Aneurysm Protects against Systemic Atherosclerosis
Hung A, Zafar M, Mukherjee S, Tranquilli M, Scoutt LM, Elefteriades JA. Carotid Intima-Media Thickness Provides Evidence that Ascending Aortic Aneurysm Protects against Systemic Atherosclerosis. Cardiology 2012, 123: 71-77. PMID: 23006774, DOI: 10.1159/000341234.Peer-Reviewed Original ResearchConceptsIntima-media thicknessCarotid intima-media thicknessAortic aneurysmCalcium scoreAortic calcium scoreAverage intima-media thicknessAortic aneurysm patientsCarotid IMT valuesDegree of atherosclerosisPositive family historyAortic aneurysm developmentDevelopment of atherosclerosisCommon carotid arterySystemic atherosclerosisAneurysm patientsIMT valuesMale genderRisk factorsCarotid arteryFamily historyMultiple linear regression analysisAtherosclerosisEarly markerAneurysm developmentAneurysms
2011
Atherosclerosis Plaque Heterogeneity and Response to Therapy Detected by In Vivo Molecular Imaging of Matrix Metalloproteinase Activation
Razavian M, Tavakoli S, Zhang J, Nie L, Dobrucki LW, Sinusas AJ, Azure M, Robinson S, Sadeghi MM. Atherosclerosis Plaque Heterogeneity and Response to Therapy Detected by In Vivo Molecular Imaging of Matrix Metalloproteinase Activation. Journal Of Nuclear Medicine 2011, 52: 1795-1802. PMID: 21969358, PMCID: PMC3235922, DOI: 10.2967/jnumed.111.092379.Peer-Reviewed Original ResearchConceptsHigh-fat dietSPECT/CTTracer uptakeMMP activationNormal chowMatrix metalloproteinasesApolipoprotein-deficient miceOil Red O stainingDevelopment of atherosclerosisMatrix metalloproteinase activationRed O stainingAtherosclerotic mouse aortasOil Red OHFD withdrawalMolecular imagingAreas of discordanceDietary modificationMacrophage infiltrationPlaque presenceMacrophage contentPlaque areaPlaque biologyAtherosclerotic plaquesMMP expressionMetalloproteinase activation
2007
Plasma insulin levels predict the development of atherosclerosis when IRS2 deficiency is combined with severe hypercholesterolemia in apolipoprotein E-null mice.
Gonzalez-Navarro H, Vila-Caballer M, Pastor M, Vinue A, White M, Burks D, Andres V. Plasma insulin levels predict the development of atherosclerosis when IRS2 deficiency is combined with severe hypercholesterolemia in apolipoprotein E-null mice. Frontiers In Bioscience-Landmark 2007, 12: 2291-8. PMID: 17127239, DOI: 10.2741/2231.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApolipoproteins EAtherosclerosisBlood GlucoseDiabetes Mellitus, Type 2Diabetic AngiopathiesFemaleHypercholesterolemiaInsulinInsulin Receptor Substrate ProteinsIntracellular Signaling Peptides and ProteinsLipidsMacrophagesMaleMiceMice, KnockoutMuscle, Smooth, VascularPhosphoproteinsConceptsInsulin receptor substrate 2ApoE-/- miceDevelopment of atherosclerosisIrs2-/- miceSevere hypercholesterolemiaInsulin levelsType 2 diabetic patientsAtherosclerotic lesion burdenPre-diabetic patientsPlasma insulin levelsFat-fed miceAbsence of hyperglycaemiaDefective insulin signalingDiabetic patientsLesion burdenClinical manifestationsInsulin resistanceModerate hypercholesterolemiaApolipoprotein EGlucose levelsAtherosclerotic lesionsAtherosclerosisHypercholesterolemiaNull miceImportant modulator
2006
Molecular Characterization of Loss-of-Function Mutations in PCSK9 and Identification of a Compound Heterozygote
Zhao Z, Tuakli-Wosornu Y, Lagace TA, Kinch L, Grishin NV, Horton JD, Cohen JC, Hobbs HH. Molecular Characterization of Loss-of-Function Mutations in PCSK9 and Identification of a Compound Heterozygote. American Journal Of Human Genetics 2006, 79: 514-523. PMID: 16909389, PMCID: PMC1559532, DOI: 10.1086/507488.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultAmino Acid SequenceCells, CulturedChild, PreschoolCholesterol, LDLFemaleHeterozygoteHumansImmunoprecipitationMaleMiddle AgedModels, MolecularMolecular Sequence DataMutation, MissensePedigreeProprotein Convertase 9Proprotein ConvertasesProtein ConformationProtein FoldingProtein TransportRecombinant ProteinsSerine EndopeptidasesConceptsProprotein convertase subtilisin/kexin type 9Low plasma levelsPlasma levelsLevels of PCSK9Function mutationsLow-density lipoprotein cholesterolConvertase subtilisin/kexin type 9Subtilisin/kexin type 9LDL-lowering therapyCoronary heart diseaseDevelopment of atherosclerosisApparent good healthCompound heterozygotesWild-type PCSK9Immunoblotting of plasmaLipoprotein cholesterolHeart diseasePCSK9 secretionType 9Confer protectionLDLGood healthElevated levelsSevere lossAttractive targetA mechanosensory complex that mediates the endothelial cell response to fluid shear stress
Tzima E, Irani‐Tehrani M, Kiosses W, Dejana E, Schultz D, Engelhardt B, Cao G, DeLisser H, Schwartz M. A mechanosensory complex that mediates the endothelial cell response to fluid shear stress. The FASEB Journal 2006, 20: a1378-a1378. DOI: 10.1096/fasebj.20.5.a1378-c.Peer-Reviewed Original ResearchPECAM-1-null miceDownstream inflammatory genesPECAM-1VE-cadherinDevelopment of atherosclerosisICAM-1 expressionNF-kB activationInitiation of atherosclerosisBlood pressureVascular remodelingHigh-affinity stateInflammatory genesNF-κBCell responsesEndothelial cell responsesNull miceMechanosensory complexIntegrin activationAffinity stateAtherosclerosisVEGFR2Heterologous cellsPathway upstreamActivationSrc family kinases
2005
Nicotine induces mitogen-activated protein kinase dependent vascular smooth muscle cell migration
Di Luozzo G, Pradhan S, Dhadwal AK, Chen A, Ueno H, Sumpio BE. Nicotine induces mitogen-activated protein kinase dependent vascular smooth muscle cell migration. Atherosclerosis 2005, 178: 271-277. PMID: 15694934, DOI: 10.1016/j.atherosclerosis.2004.09.017.Peer-Reviewed Original ResearchConceptsVascular smooth muscle cell migrationSmooth muscle cell migrationMuscle cell migrationInhibitors of p38VSMC migrationMitogen-activated protein kinaseEndothelial cellsDevelopment of atherosclerosisEffects of nicotineCell migrationWestern blotting methodInjury modelVascular endotheliumCigarette smokeBoyden chamber chemotaxis assaysAortic VSMCsChemotactic effectMAPKs p38NicotineChemoattractant moleculesChemotaxis assaysCellular mechanismsUltrastructural changesVSMCP44/42 activation
2002
Estradiol suppresses vascular monocyte chemotactic protein-1 expression during early atherogenesis
Seli E, Kayisli UA, Selam B, Seli M, Arici A. Estradiol suppresses vascular monocyte chemotactic protein-1 expression during early atherogenesis. American Journal Of Obstetrics And Gynecology 2002, 187: 1544-1549. PMID: 12501061, DOI: 10.1067/mob.2002.127306.Peer-Reviewed Original ResearchConceptsMonocyte chemotactic protein-1 expressionChemotactic protein-1 expressionProtein-1 expressionLipid depositionSerum total cholesterol concentrationVascular lipid depositionProtein 1 antibodyAorta of animalsTotal cholesterol concentrationDevelopment of atherosclerosisSmooth muscle cellsPlacebo pelletsAtherogenic stimuliDeficient miceMacrophage recruitmentEarly atherogenesisImmunohistochemical analysisTreatment groupsC57BL/6 backgroundCholesterol concentrationsMuscle cellsArterial wallB stainingAortaEstradiol
1998
Aminoguanidine has an anti-atherogenic effect in the cholesterol-fed rabbit
Panagiotopoulos S, O'Brien R, Bucala R, Cooper M, Jerums G. Aminoguanidine has an anti-atherogenic effect in the cholesterol-fed rabbit. Atherosclerosis 1998, 136: 125-131. PMID: 9544739, DOI: 10.1016/s0021-9150(97)00192-5.Peer-Reviewed Original ResearchConceptsAdvanced glycosylation endproductsAortic archAbdominal aortaAdvanced glycationPlaque formationVasculopathy of diabetesAnti-atherogenic effectsHigh-cholesterol dietCholesterol-fed rabbitsDevelopment of atherosclerosisDegree of atheromaCholesterol dietAortaAtheromaRabbitsThoracicAminoguanidineDosesGlycationTreatmentArchAge levelsNon-enzymatic interactionVasculopathySudan IV
1997
17 beta-estradiol regulation of human endothelial cell basal nitric oxide release, independent of cytosolic Ca2+ mobilization.
Caulin-Glaser T, García-Cardeña G, Sarrel P, Sessa W, Bender J. 17 beta-estradiol regulation of human endothelial cell basal nitric oxide release, independent of cytosolic Ca2+ mobilization. Circulation Research 1997, 81: 885-92. PMID: 9351464, DOI: 10.1161/01.res.81.5.885.Peer-Reviewed Original ResearchConceptsHuman umbilical vein endothelial cellsEstrogen receptorCytosolic Ca2ENOS activityBasal nitric oxide releaseEndothelial NO synthase activityCardiovascular protective roleNO synthase activityDevelopment of atherosclerosisFemale human umbilical vein endothelial cellsNitric oxide releaseCritical effector moleculeUmbilical vein endothelial cellsVein endothelial cellsCardiovascular protectionEstradiol exposureAnimal modelsCGMP formationProtective roleOxide releaseEndothelial cellsNO releaseE2Physiological concentrationsEffector molecules
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