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2 Mechanisms of OS-induced nerve damage In the context of DN, OS contributes to oxidase activation, mitochondrial dysfunction, apoptosis, inflammation, and endoplasmic reticulum (ER) stress, which are critical in the pathogenesis of nerve injury (Figure 1)

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Enhancement by homocysteine of plasminogen activator inhibitor-1 gene expression and secretion from vascular endothelial and smooth muscle cells