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649 However, neither intravenous nor intracerebroventricular administration alone fully improved the clinical phenotype, indicating limitations in standard AAV vector transduction

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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