Figure 1.

The effects of PPARγ activation on reactive oxygen species and nitric oxide production in the vascular wall. Factors including hypoxia and shear stress increase the production of superoxide in the vascular wall by NADPH oxidase. Superoxide $\left({\text{O}}_2^{{\cdot }^{-}}\right)$ rapidly reacts with nitric oxide (NO) generated by endothelial nitric oxide synthase (eNOS) to reduce the bioavailability of NO to stimulate vasodilation and inhibit vascular smooth muscle cell (VSMC) proliferation, platelet activation, and adhesion molecule expression. PPARγ activation inhibits NADPH oxidase expression and activity [61] and stimulates NO production in vascular endothelial cells (EC) [58, 59]. These effects illustrate potential mechanisms by which PPARγ activation may favorably modulate pulmonary endothelial dysfunction and pulmonary hypertension.