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- W2065683143 abstract "In addition to inducing tumor cell apoptosis, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) shows broad biological functions both in vitro and in vivo. TRAIL gene deletion enhanced atherogenesis in hyperlipidemic mice, supporting that endogenous TRAIL has protective actions in maintaining blood vessel homeostasis and repressing atherosclerosis. The mechanisms of this beneficial effect are not understood. It remains to be determined whether the athero-protective action of TRAIL is via direct impacts on residential vascular cells or indirectly by modulating systemic immune functions. However, in vitro experiments indicate that excessive TRAIL may stimulate endothelial cell apoptosis, smooth muscle proliferation and migration, and inflammatory responses. Moreover, TRAIL can stimulate lipid uptake and foam cell formation in cultured macrophages. Here we provide a critical review on the potential relationships between TRAIL and atherosclerosis. We propose that increased TRAIL production may also have potential detrimental effects on vascular inflammation and atherosclerosis. Further in vivo experiments are warranted to elucidate the effects of exogenous TRAIL on atherogenesis." @default.
- W2065683143 created "2016-06-24" @default.
- W2065683143 creator A5004923438 @default.
- W2065683143 creator A5004990725 @default.
- W2065683143 creator A5034953747 @default.
- W2065683143 creator A5061835895 @default.
- W2065683143 date "2014-12-01" @default.
- W2065683143 modified "2023-10-15" @default.
- W2065683143 title "Tumor necrosis factor-related apoptosis-inducing ligand in vascular inflammation and atherosclerosis: A protector or culprit?" @default.
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