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Thus, OS in DM represents a paradigm of metabolic memory, where initial oxidative damage perpetuates dysfunction long after glycemic control is achieved, underscoring the need for early redox-targeted therapies

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SVV 3C pro plasmids with protease activity mutations (GFP-3 C-H48A, GFP-3 C-C160A, and GFP-3 C-DM) showed that 3C pro -mediated degradation was protease activity-dependent (Fig