title: Cardiac and vascular phenotypes in the apolipoprotein E-deficient mouse.
abstract: Cardiovascular death is frequently associated with atherosclerosis, a chronic multifactorial disease and a leading cause of death worldwide. Genetically engineered mouse models have proven useful for the study of the mechanisms underlying cardiovascular diseases. The apolipoprotein E-deficient mouse has been the most widely used animal model of atherosclerosis because it rapidly develops severe hypercholesterolemia and spontaneous atherosclerotic lesions similar to those observed in humans. In this review, we provide an overview of the cardiac and vascular phenotypes and discuss the interplay among nitric oxide, reactive oxygen species, aging and diet in the impairment of cardiovascular function in this mouse model.
authors.affiliation: Department of Physiological Sciences, Health Sciences Center, Federal University of Espirito Santo, Vitoria, ES, Brazil. evasquez@pq.cnpq.br
authors.forename: Elisardo C
authors.initials: EC
authors.lastname: Vasquez
authors.forename: Veronica A
authors.initials: VA
authors.lastname: Peotta
authors.forename: Agata L
authors.initials: AL
authors.lastname: Gava
authors.forename: Thiago Mc
authors.initials: TM
authors.lastname: Pereira
authors.forename: Silvana S
authors.initials: SS
authors.lastname: Meyrelles
mesh_terms: D000375:Aging; D000818:Animals; D001057:Apolipoproteins E / Q000172:deficiency* / Q000235:genetics; D050197:Atherosclerosis / Q000235:genetics / Q000473:pathology*; D001808:Blood Vessels / Q000473:pathology; D004032:Diet; D004195:Disease Models, Animal; D006321:Heart / Q000503:physiopathology*; D006439:Hemodynamics; D006952:Hyperlipoproteinemia Type III / Q000235:genetics / Q000473:pathology*; D051379:Mice; D009569:Nitric Oxide / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D001057:Apolipoproteins E; D017382:Reactive Oxygen Species; D009569:Nitric Oxide