The aim of the study was to characterize cardiovascular aging with functional (Doppler) and molecular (RT-qPCR and immunohistochemistry quantifications) approaches using three murine models. Molecular studies on aorta (AO) and mesenteric arteries (MA) were used to explore the role of oxidative stress and inflammation. Time-induced aging model corresponded to 25 months-old C57Bl/6J mice feed with standard diet. Doppler exhibited a concentric left ventricle hypertrophy with a decreased aortic distensibility, and an increased aortic thickening. This model presented both a decreased Thioredoxin1 expression (AO and MA) and an increased NADPH oxidase (MA) expression. Inflammation markers were increased in MA (IL-1beta in MA and in AO (IL-6, TNF-alpha). Three months with High Fat and Protein Diet (HFPD) at 9 months induce a major hyperlipidemia. This model exhibited a dilated cardiopathy with both a decreased aortic distensibility and an increased aortic thickening. HFPD increased NADPH oxidase, IL1-beta and TNF-alpha expressions and decreased Thioredoxin1 expression (AO and MA). The mixed model corresponded to 25-months old C57Bl/6J mice feed for 3 months with HFPD. They presented a major cardiopathy with a decreased aortic distensibility, and exhibited both a major oxidative stress (increased NADPH oxidase and decreased Thioredoxin1 in AO and MA) and a major endothelial inflammation (increased IL-1beta, IL-6 and TNF-alpha in AO and MA). eNOS gene was not modify in any model. We conclude that NADPH oxidase and Thioredoxin1 seem to play a key role in the arterial aging process and might be interesting potential targets for therapeutics assays.