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Itaconate, derived from citrate produced in the TCA cycle, contains ,-unsaturated carboxylic acid, and covalently modifies at the Cys151 residue of Keap1 (78)

This suggests that a resistance exercise-related mechanism of inducing plasma NO, perhaps due to increased shear stress that triggered an up-regulation in NO-cGMP signaling, is a conceivable candidate for this response

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