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In nonalcoholic fatty liver disease, endogenous denatured DNA, cholesterol, and HMGB1 derived from apoptotic and necrotic host cells, together with mtDNA, formylated peptides, and ATP released due to mitochondrial dysfunction, induce inflammation by activating the cGAS/STING pathway and NLRP3 inflammasomes [267]

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FOXO4-DRI has a circulating half-life of approximately 24 hours (based on similar peptide pharmacokinetics), but its intracellular effects persist for 4872 hours once the FOXO4p53 interaction is disrupted