Research Paper Volume 15, Issue 1 pp 164—178
Doxorubicin induced ROS-dependent HIF1α activation mediates blockage of IGF1R survival signaling by IGFBP3 promotes cardiac apoptosis
Figure 6. Graphical representation illustrating the mechanism underlying Dox-induced cell apoptosis. Dox induced ROS generation, which suppressed PHD. This stabilized nuclear HIF1A, promoted IGFBP3, and enhanced its extracellular association with IGF1. This interaction blocked survival signaling and resulted in cell apoptosis.