Figure 2.

Scheme showing the possible pathways from hepatic damage to fibrosis leading to cancer. The oxidative stress and ROS production follow mitochondrial dysfunction and hepatic damage. The direct consequences are impairment of deiodinase activity leading to decreased T3 production, on the other hand deiodinase 3 is imbalanced with increased activity and increased rT3, which stimulates the proliferation of tumor cells. The ROS produced give rise to inflammatory cytokines that increase the ROS and activate Hepatic Stellate Cells (HSC), leading to fibrosis and eventually cancer. The inhibition by tetrac of the fibrogenic process is only suggested as shown by the question mark, with integrin αvβ3 being among the ECM components involved in the “activation” of the Hepatic Stellate Cells.