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Free radicals contribute to heart failure through direct damage to cardiomyocytes, mitochondrial dysfunction, and the promotion of fibrosis

16, 17 Under conditions of BH 4 deficiency, electron flow from the reductase domain to the oxidase domain is diverted to molecular oxygen rather than to L-arginine, a substrate of NO, leading to eNOS uncoupling

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Only through such efforts can we achieve the target diagnostic ensitivity/specificity of 80% essential for cost-effective, stage-specific DPN management

This upregulation of vWF expression on endothelial cells in response to proinflammatory stimuli aligns with previous findings 57