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However, in PEM patients, due to a lack of effective negative feedback regulation (e.g., compromised antioxidant capacity and impaired mitochondrial autophagy), these responses fail to resolve post-exercise, thereby potentially progressing into a chronic pathological state (105) ( Figure 2 )

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Collectively, our findings establish a novel link between the oncogene VRK2 and GSH synthesis metabolism, providing a molecular basis for developing stratified metabolic therapies for PC patients

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Thus, an inability to biosynthesize EGT appears to lead to attenuated gliotoxin production compared to wild-type