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ROS overproduction-induced oxidative stress represents a principal mechanism of endothelial cell death, with ROS activating multiple pathways leading to endothelial cell demise

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Additionally, activation of the aryl hydrocarbon receptor (AHR) signaling pathway has been implicated in the transcriptional and possibly epigenetic regulation of both CYP27B1 and CYP24A1 (14, 15)

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