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Despite initial enthusiasm for cuproptosis as a novel pathogenetic mechanism [27,51,54] , the molecular and metabolic complexities underlying copper-dependent hepatocellular injury in Wilson disease remain unresolved, especially since the role of ROS and reactive copper intermediates was not originally included in the cuproptosis framework [51,54]

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TB-500 (Thymosin Beta-4 Fragment) Origin: Synthetic version of a naturally occurring peptide present in most human cells