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Description

Excessive ROS disrupt the oxidation-antioxidant balance, activate inflammatory cell signals, and induce endothelial cell dysfunction through mitochondria-mediated apoptosis, promoting vascular smooth muscle cell proliferation, interfering with nitric oxide synthesis, and delaying endothelial repair, thereby accelerating atherosclerosis development (Tullio et al., 2013

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NAG safety considerations NAG may be shellfish-derived or produced by another route

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Gomes C

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Further information on research design is available in the Reporting Summary linked to this article

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