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 9
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