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Levels of active G6PD are regulated at both the transcriptional level via various canonical signaling pathways (e.g., JAK-STAT, Wnt, mTOR), and at the post-translational level (e.g., via phosphorylation, de-acetylation), allowing tight coordination of G6PD activity to meet acute cellular demand in response to oxidative stress, metabolic demand, or systemic inflammation ( Figure 1A-1 )
This paper aims to synthesize current knowledge regarding the potential role of HHcy in neurodegenerative diseases, drawing compelling connections among dietary methionine daily consumption, HHcy, oxidative stress, mitochondrial functioning, and accelerated epigenetic aging
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