2023
Efficacy and safety of alirocumab in children and adolescents with heterozygous familial hypercholesterolaemia inadequately controlled with statins
Santos R, Wiegman A, Caprio S, Cariou B, Averna M, Poulouin Y, Scemama M, Manvelian G, Garon G, Daniels S. Efficacy and safety of alirocumab in children and adolescents with heterozygous familial hypercholesterolaemia inadequately controlled with statins. European Heart Journal 2023, 44: ehad655.2809. DOI: 10.1093/eurheartj/ehad655.2809.Peer-Reviewed Original ResearchProprotein convertase subtilisin/kexin type 9Safety of alirocumabKey secondary endpointHeterozygous familial hypercholesterolaemiaWeek 24Secondary endpointsPediatric patientsLipid parametersFamilial hypercholesterolaemiaTreatment periodTreatment groupsInternational phase 3 trialConvertase subtilisin/kexin type 9Subtilisin/kexin type 9Atherogenic lipid parametersEfficacy of alirocumabMean baseline LDLOpen-label periodPhase 3 trialLDL cholesterol levelsSignificant treatment differencesAlirocumab treatmentBaseline LDLPlacebo Q2WWeek 104Pharmacologic and Genetic Downregulation of Proprotein Convertase Subtilisin/Kexin Type 9 and Survival From Sepsis
Lawler P, Manvelian G, Coppi A, Damask A, Cantor M, Ferreira M, Paulding C, Banerjee N, Li D, Jorgensen S, Attre R, Carey D, Krebs K, Milani L, Hveem K, Damås J, Solligård E, Stender S, Tybjærg-Hansen A, Nordestgaard B, Hernandez-Beeftink T, Rogne T, Flores C, Villar J, Walley K, Liu V, Fohner A, Lotta L, Kyratsous C, Sleeman M, Scemama M, DelGizzi R, Pordy R, Horowitz J, Baras A, Martin G, Steg P, Schwartz G, Szarek M, Goodman S. Pharmacologic and Genetic Downregulation of Proprotein Convertase Subtilisin/Kexin Type 9 and Survival From Sepsis. Critical Care Explorations 2023, 5: e0997. PMID: 37954898, PMCID: PMC10635596, DOI: 10.1097/cce.0000000000000997.Peer-Reviewed Original ResearchProprotein convertase subtilisin/kexin type 9Convertase subtilisin/kexin type 9Subtilisin/kexin type 9Human cohort studiesODYSSEY OUTCOMESCohort studyType 9Isotype-matched controlExperimental murine modelSepsis ratePCSK9 inhibitionPCSK9 inhibitorsSepsis complicationsSepsis mortalitySepsis outcomeImproved survivalBacterial sepsisClinical outcomesBloodstream clearanceSepsis modelClinical trialsOdds ratioCardiovascular diseasePretreatment settingSepsis diagnosis
2021
PCSK9 Activity Is Potentiated Through HDL Binding
Burnap SA, Sattler K, Pechlaner R, Duregotti E, Lu R, Theofilatos K, Takov K, Heusch G, Tsimikas S, Fernández-Hernando C, Berry SE, Hall WL, Notdurfter M, Rungger G, Paulweber B, Willeit J, Kiechl S, Levkau B, Mayr M. PCSK9 Activity Is Potentiated Through HDL Binding. Circulation Research 2021, 129: 1039-1053. PMID: 34601896, PMCID: PMC8579991, DOI: 10.1161/circresaha.121.319272.Peer-Reviewed Original ResearchConceptsProprotein convertase subtilisin/kexin type 9High-density lipoproteinSmall high-density lipoproteinHDL proteomeApolipoprotein C3Low-density lipoprotein receptor degradationPlasma proprotein convertase subtilisin/kexin type 9Convertase subtilisin/kexin type 9Subtilisin/kexin type 9Coronary artery diseaseLow-density lipoprotein uptakeArtery diseasePostprandial lipaemiaBruneck StudyPCSK9 levelsPostprandial responseTriglyceride levelsPlasma levelsApolipoprotein profilesSAPHIR studyIndependent cohortPhospholipid transfer proteinMagnetic resonancePCSK9 activityType 9PCSK9 Inhibiting Monoclonal Antibodies
Ahmed Z, Juthani P, Lee M, Desai N. PCSK9 Inhibiting Monoclonal Antibodies. Stroke Revisited 2021, 125-133. DOI: 10.1007/978-981-16-3923-4_11.Peer-Reviewed Original ResearchProprotein convertase subtilisin/kexin type 9Lipid-lowering medicationsSubset of patientsIschemic strokeLower PCSK9Low-density lipoprotein cholesterolConvertase subtilisin/kexin type 9Subtilisin/kexin type 9Monoclonal antibodiesCoenzyme A (HMG-CoA) reductase inhibitorsComponents of dyslipidemiaHigh-intensity statinsStroke risk reductionModifiable risk factorsHealthy lifestyle modificationsLDL-C levelsRisk of strokeStatin-induced myopathyTreatment of hyperlipidemiaA Reductase InhibitorsLifestyle modificationStatin useLipoprotein cholesterolPCSK9 inhibitorsStroke outcome
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 target
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