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- W2806949619 abstract "The current study focused on the metabolic effects of LTB4 on endothelial and mitochondrial functions in human aortic endothelial cells (HAECs). LTB4 treatment in a dose-dependent manner augmented the degree of mitochondrial superoxide generation in HAECs. Such impairments in mitochondrial integrity and dynamics by increased dynamin-related protein-1 (Drp1) and fission-1 (Fis1) protein expression but, reduced mitofusin (Mfn)-1 protein expression was noticed in HAECs. Furthermore, LTB4 considerably augmented the expression of Cytochrome C and Bax, but diminished the expression of Bcl-2, thus promoting endothelial apoptosis and inflammation. Additionally, LTB4 treatment resulted in the suppression of phosphatidyl inositol 3- kinase (PI3K)/Akt signaling. Finally, severe vascular oxidative damage and mitochondrial impairments in aorta of transgenic mice expressing human LTB4 (LTB4-Tg) mice were observed compared to wild-type C57BL/6 J mice. Overall, the current investigation discovers a novel mechanism through which LTB4 leads to vascular oxidative damage and mitochondrial dysfunction, resulting further understanding of the mechanisms responsible for the effects of LTB4 in the progression of atherosclerosis." @default.
- W2806949619 created "2018-06-13" @default.
- W2806949619 creator A5087999921 @default.
- W2806949619 date "2018-06-01" @default.
- W2806949619 modified "2023-09-27" @default.
- W2806949619 title "Leukotriene B4 Mediates Vascular Oxidative Stress and Mitochondrial Dysfunction in Human Aortic Endothelial Cells" @default.
- W2806949619 doi "https://doi.org/10.1016/j.atherosclerosissup.2018.04.344" @default.
- W2806949619 hasPublicationYear "2018" @default.
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