Research Paper Volume 5, Issue 7 pp 515—530

Oxidative stress improves coronary endothelial function through activation of the pro-survival kinase AMPK

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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.