Figure 7. Schematic figure of the role of PKG in the vascular injury.

In the uninjured vessels, intact endothelial cells produce NO, which activates PKG in VSMCs and platelets, leading to inhibition of proliferation and aggregation. After vascular injury, EC denudation decreases NO production, resulting in the decreased level of PKG in VSMCs and platelets. In addition, activated platelets produce PDGF which can activate VSMCs. All these processes contribute to VSMC proliferation and platelet activation. In contrast, Exisulind treatment can prevent the decrease of PKG activity in VSMCs and platelets, leading to inhibition of both cells in conjunction with facilitating re-endothelialization.