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The knockout of Nrf2 can significantly reduce the protein expression levels of SLC7A11 and HO-1, and can promote the accumulation of lipid peroxides, trigger ferroptosis through iron overload, excess ROS generation and lipid peroxidation, and aggravate the progression of AS

NO generated in endothelial cells diffuses rapidly to adjacent smooth muscle cells, which activates soluble guanylate cyclase (sGC) and allows the conversion of GTP to cyclic GMP, initiating a signaling cascade leading to vasodilation [8, 9]

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