Research Paper Volume 5, Issue 7 pp 515—530
Oxidative stress improves coronary endothelial function through activation of the pro-survival kinase AMPK
Figure 8. Model for EC-specific ROS-mediated improvement in endothelial function. Nox2-induced ROS in vascular endothelium activates CaMKKβ-AMPK, which in turn, activates eNOS to induce NO-mediated vasodilatation and inhibits mTOR resulting in protective autophagy.