Mitohormesis: another pleiotropic effect of statins?

This editorial refers to ‘Opposite effects of statins on mitochondria of cardiac and skeletal muscles: a ‘mitohormesis’ mechanism involving reactive oxygen species and PGC-1’†, by J. Bouitbir et al., on page 1397 The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors or statins are some of the most widely prescribed drugs in the world for the primary and secondary prevention of cardiovascular disease. Most, if not all, of the benefits of statins could be attributed to the reduction in serum cholesterol levels. Indeed, decreases in LDL-cholesterol with statin therapy correlate almost linearly with reductions in cardiovascular events.1 In addition, recent experimental studies and clinical trials suggest that statins may exert some of their cardiovascular benefits beyond cholesterol lowering, i.e. pleiotropic effects.2 Some of these non-cholesterol benefits include improvement in endothelial function, anti-inflammatory and antioxidative effects.3 Whether these pleiotropic effects of statins actually contribute to cardiovascular risk reduction in clinical trials, however, remains to be determined.