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The Tat-SIRT5-CTM peptide specifically blocked the interaction of SIRT5 with ANXA1, led to SIRT5 degradation and thereby inhibiting SIRT5-mediated desuccinylation of ANXA1, which in turn alleviated microglia-induced neuroinflammation, and eventually improved the survival of neurons subjected to cerebral ischemia and reperfusion injury.
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