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The primary mechanical injury in TBI triggers secondary injury cascades involving neuroinflammation, oxidative stress, mitochondrial dysfunction, and excitotoxicity

Central to these processes is the improper activation of crucial signaling pathways, such as transforming growth factor (TGF-)/suppressor of mothers against decapentaplegic homolog (Smad), Wnt/-catenin, and Hedgehog signaling, accompanied by profound metabolic reprogramming and epigenetic remodeling

This poor absorption profile means that patients taking standard glutathione capsules must consume massive doses over many months to see even marginal increases in intracellular antioxidant levels

Enzyme-responsive prodrugs require meticulous optimization of enzymes and their substrates

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