2023
Overexpression of NgBR inhibits high-fat diet–induced atherosclerosis in ApoE-deficiency mice
Gong K, Wang M, Wang D, Gao Y, Ma L, Yang X, Zhu X, Chen S, Zhang M, Li H, Chen Y, Hu W, Miao Q, Iwakiri Y, Liao C, Duan Y, Han J. Overexpression of NgBR inhibits high-fat diet–induced atherosclerosis in ApoE-deficiency mice. Hepatology Communications 2023, 7: e0048. PMID: 36996002, PMCID: PMC10069848, DOI: 10.1097/hc9.0000000000000048.Peer-Reviewed Original ResearchConceptsNgBR overexpressionScavenger receptor type BIHigh-fat diet-induced atherosclerosisApolipoprotein E deficient miceApoE deficiency miceApoE-/- miceDiet-induced atherosclerosisHigh-fat dietLevels of cholesterolBile acid synthesisCholesterol synthesis genesInflammatory factorsVascular inflammationProtein kinase αSinus lesionsHepatic steatosisAortic rootRisk factorsDeficient miceAtherosclerosis treatmentFree fatty acidsCholesterol metabolismAtherosclerosisAcid synthesisAAV injection
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