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• W2022101330 abstract "Several experimental and clinical studies have shown that oxidized low-density lipoprotein and oxidation-sensitive mechanisms are central in the pathogenesis of vascular dysfunction and atherogenesis. Here, we have used p66 Shc−/− and WT mice to investigate the effects of high-fat diet on both systemic and tissue oxidative stress and the development of early vascular lesions. To date, the p66 Shc−/− mouse is the unique genetic model of increased resistance to oxidative stress and prolonged life span in mammals. Computer-assisted image analysis revealed that chronic 21% high-fat treatment increased the aortic cumulative early lesion area by ≈21% in WT mice and only by 3% in p66 Shc−/− mice. Early lesions from p66 Shc−/− mice had less content of macrophage-derived foam cells and apoptotic vascular cells, in comparison to the WT. Furthermore, in p66 Shc−/− mice, but not WT mice, we found a significant reduction of systemic and tissue oxidative stress (assessed by isoprostanes, plasma low-density lipoprotein oxidizability, and the formation of arterial oxidation-specific epitopes). These results support the concept that p66 Shc−/− may play a pivotal role in controlling systemic oxidative stress and vascular diseases. Therefore, p66 Shc might represent a molecular target for therapies against vascular diseases." @default.
• W2022101330 created "2016-06-24" @default.
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• W2022101330 date "2003-02-05" @default.
• W2022101330 modified "2023-10-01" @default.
• W2022101330 title "Deletion of the p66 ^Shc longevity gene reduces systemic and tissue oxidative stress, vascular cell apoptosis, and early atherogenesis in mice fed a high-fat diet" @default.
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• W2022101330 doi "https://doi.org/10.1073/pnas.0336359100" @default.
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