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 angiotensin