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Elevated oxygen availability in hyperoxic states bolsters ROS generation through NOX activity [355]

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These findings were supported by the relaxation of large vessels (ex vivo), mainly by acting on vascular endothelial cells but also on vascular smooth muscle cells, increasing NO production and migration of endothelial cells, activating the signal pathways of Src, Cav-1, and eNOS, and reducing proteinprotein interaction between eNOS and Cav-1 [121,122]