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The ATM/AKT pathway is a compensatory mechanism to cope with the ROS accumulation induced by the inhibition of the Trx system in colon cancer [40]

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DAMPs such as HMGB1, IL-33, and ATP released from liver injury bind to TLR2/4 and activate hepatic stellate cells (HSC), prompting their transformation into myofibroblasts and secretion of a large number of extracellular matrix proteins, which leads to matrix deposition and fibrosis [277, 316, 317]

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