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It has also been confirmed that SIN phosphorylates p62 at the Ser351 site (corresponding to Ser349 in humans), leading to the degradation of Keap1 and upregulation of Nrf2 expression
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A fundamental defect in the M2-polarization program itself exists, rooted in the diabetes-induced mitochondrial damage that cripples the specific bioenergetic infrastructure required for alternative activation
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