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Hus findings suggest that GLS2 may be a mediator to p53 s role in energy metabolism and antioxidant defense, ultimately contributing to its tumor suppression abilities

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Mitochondrial dysfunction can contribute to mitochondrial DNA (mtDNA) mutations, increased mitochondrial reactive oxygen species (mtROS), and oxidative stress, which have been progressively underscored in the pathogenesis of RA over recent years (9)

Moreover, studies have indicated that human ApoE glycans undergo sialic acid modification or sialylation, a structural alteration found to be more prominent in ApoE derived from the brain and CSF than plasma