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Deletion of Mat1a promotes liver injury Deletion of Mat1a enhances the susceptibility to liver injury in mice ( Mat1a - / - mice ( All of the above suggest that abnormal dietary intake and defective metabolism of Met could result in the abnormal levels of Met and its metabolites (SAMe and GSH) and accumulation of toxic metabolic intermediates (Hcy, Hcythiolactone, and 3-MTP) in the liver, which in turn affects the functions and the inflammatory responses to damage/infection of the liver (Figure 4)

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