Figure 10. Statin effects on the cardiac myocyte.

The main cholesterol synthesis pathway is highlighted in grey. The impact of statin inhibition of HMG-CoA reductase, the rate limiting step of cholesterol synthesis, is shown. Statins limit production of cholesterol and isoprenoid intermediates (FPP, GGPP). The latter are responsible for post-translational modification of a number of proteins including those of the small G protein family (Ras, Rho, Rac). The potential roles of isoprenoid- and cholesterol-dependent changes in modulating cardiac myocyte function are listed. From the present study, bold text indicates established effects, whereas grey text denotes effects which have been eliminated. ROS reactive oxygen species (which reduce bioavailable NO); PP phosphatase; AC adenylyl cyclase. See Discussion for detailed mechanisms and references.