Biochemical and Biophysical Research Communications
Regular ArticleIncreased Plasma and Lipoprotein Lipid Peroxidation in apo E-Deficient Mice
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2019, Neurobiology of StressCitation Excerpt :Fourth, another relevant aspect of APOE is its protective role in oxidative stress. Specifically, a significant increase in lipid peroxidation in plasma and lipoprotein was observed in mice with APOE ablated (Hayek et al., 1994). Furthermore, APOE ε4 confers higher risk of cell death compared to APOE ε2 in when cells are exposed to hydrogen peroxide. (
Role of Nrf2 in the pathogenesis of atherosclerosis
2015, Free Radical Biology and MedicineCitation Excerpt :Nrf2 modulates gene expression involved in GSH homeostasis, such as glutamate-cysteine ligase modifier subunit and catalytic subunit (GCLM and GCLC, respectively), glutathione reductase (GR) and glutathione peroxidase (GPx). In ApoE KO mice, a decrease in GSH and increase in oxidative stress is associated with atherosclerosis development [48–50]. In addition, GSH deprivation accelerates, while liposomal GSH administration attenuates, atherosclerosis development in ApoE KO mice, suggesting that GSH has protective effect against atherosclerosis [51,52].
The influence of apoE-deficiency and LDL-receptor-deficiency on the HDL subpopulation profile in mice and in humans
2014, AtherosclerosisCitation Excerpt :Eliminating apoE in mice results in a significant decrease of lipidated HDL particles and, presumably, a loss of all functions associated with them. This hypothesis is in line with others' findings that apoE−/− mice have decreased anti-inflammatory, anti-oxidative capacities and HDL from these mice has decreased cholesterol efflux capacity [20–22]. Therefore, results generated in apoE−/− mice cannot be extrapolated to humans without taking these substantial differences into consideration.
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