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Together these results indicate that the succination of GSH, but not its detoxification, is responsible for the oxidative stress observed in Fh1-deficient cells GSH succination increases GSH biosynthesis We hypothesized that the chronic depletion of GSH caused by succination could perturb cell metabolism and contribute to a general deregulation of redox homeostasis

The unbiased, consecutive recruitment may have introduced different disease endotypes or subtypes

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2b), in agreement with our previous characterization of this BBB model [40]