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Ultimately, this review proposes that PEM may arise from a complex interplay among mitochondrial dysfunction, immune activation, and neuroinflammation, which together form a self-perpetuating loop of energy exhaustion - inflammation amplification, potentially contributing to the chronic and multi-system nature of PEM symptoms

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This is a mechanism to protect sensitive protein thiols from irreversible oxidation and may also serve to prevent loss of GSH under oxidative conditions (Figure 2)

The C-terminal small domain, which encompasses residues 322480, undergoes a folding process that results in an sandwich [24, 28, 30]