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During the early stages of APAP-induced liver injury, stressed and damaged hepatocytes release various endogenous DAMPs, such as HMGB1, 75 nuclear DNA fragments, 76 uric acid, 77 mitochondrial DNA, 76 ATP, and heat shock protein-70, an inducible stress response protein that is translocated to the cell surface and released during cellular stress or necrotic death

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Fragmentation pathways may involve cleavage at amide bonds, producing characteristic fragment ions corresponding to partial backbone structures

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Interestingly, the abundance of bifidobacteria tended to decrease when cardiovascular events occurred, and conversely, their abundance was upregulated when CVD was ameliorated 13,14,15