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At the early stage of MS pathogenesis, vascular endothelial damage and apoptosis upregulate vasoactive substances, prompting the migration of immune cells towards the vasculature and peripheral tissues, leading to inflammation, oxidative stress, and tissue hypoxia (162, 172, 173)

However, under pathological conditions, this homeostasis is disrupted, and dysregulated ROS levels can lead to cell dysfunction or death by directly damaging biological macromolecules such as nucleic acids, membrane lipids, and proteins

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