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Neuron-specific SQOR overexpression has been shown to decrease the volume of cerebral infarction after stroke ( 2 S with hydroxocobalamin protects mitochondrial function in ischemic brain tissue by preventing H 2 S from inhibiting Complex IV ( 2 S and generates thiolate anions, significantly alleviating ischemic brain injury in mice ( 2 S production has proven beneficial: for example, oral metronidazole (to eliminate H 2 S-producing gut microbes) or a low-sulfur diet reversed neuro-metabolic abnormalities in SQOR-deficient mice (Figure 3 illustrates the diverse roles of SQOR in several systemic diseases

In addition, the use of AKT inhibitors in combination with extracellular asparagine (ASN) depletion can significantly inhibit tumor growth (Fig

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Collectively, these studies emphasize that antioxidant and nutritional interventions, while mechanistically promising, require more rigorous, biomarker-guided, and adequately powered clinical trials before definitive conclusions regarding their efficacy in post-stroke recovery can be established