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Key sources of ROS include NOXs activation, uncoupled endothelial nitric oxide synthase (eNOS), and mitochondrial dysfunction, all of which are exacerbated by hypertensive stimuli such as Ang II and mechanical shear stress

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Specifically, exposure to pro-inflammatory cytokines such as TNF-α and IFN-γ upregulates the CYP27B1 gene, which is responsible for synthesizing 1,25D, thereby promoting an anti-inflammatory effect [134]