FIGURE 6.

The proposed model of Cox4i2 mediates an increase in ROS, ferroptosis, and apoptosis in HHV7-induced RSC96 cells. HHV7 infection increases the concentrations of the ROS, increasing oxidative stress via the activation of Cox4i2. On the one hand, Cox4i2 facilitates the intracellular iron overload and redox imbalance and induces ferroptosis. On the other hand, the upregulation of oxidative stress induced by Cox4i2 activates caspase3 by regulating the ERK signalling pathway and promotes apoptosis. The arrows indicate a positive action.