fig3

Figure 3. Schematic representation of the potential connectors associated with MASH development and progression in the context of copper toxicity. In addition to cuproptosis, a novel pathway of cell death linked to excess copper, other pathomechanisms may be involved. These include excess oxidative stress, impaired energy homeostasis due to mitochondrial dysfunction, and macrophage activation with mechanisms that are not well understood. MASH: Metabolic dysfunction-associated steatohepatitis; FXR: farnesoid X receptor; ROS: reactive oxygen species.