The mechanisms mediating statin myopathy are unclear, but possibilities include decreased sarcolemmal or endoplasmic reticulum cholesterol, reduced production of prenylated proteins including the mitochondrial electron transport protein coenzyme Q10, reduced fat catabolism, increased myocellular concentrations of cholesterol and plant sterols, failure to repair damaged skeletal muscle, vitamin D deficiency, and inflammation. Increasingly, interest has focused on altered cellular energy use and mitochondrial dysfunction, with the dysfunction activating pathways leading to muscle atrophy. Although the mechanisms are poorly understood, some statins (simvastatin, atorvastatin, fluvastatin) have been shown to reduce skeletal muscle mitochondrial content and oxidative capacity in humans.