The pleiotropic effects of statins in the prevention of atherosclerosis: Editorial to: 'simvastatin suppresses apoptosis in vulnerable atherosclerotic plaques through regulating the expression of p53, Bcl-2 en Bcl-xL' by Weiwei Qin et al.

摘要

Statins, as the biggest selling class of pharmaceutical compounds, have become the cornerstone of medical treatment for hypercholesterolemia and have led to a marked reduction in morbidity and mortality from adverse cardiovascular diseases (CVD). They were initially isolated and identified as metabolites of red rice yeast [1, 2] to inhibit the rate-limiting step of cholesterol biosynthesis, the conversion of HMG-CoA to L-mevalonic acid, through blocking the activity of 3-hydroxy-3-methylglutaryl coen-zyme A reductase (HMG CoA-reductase) [3]. This leads to decreased hepatic cholesterol biosynthesis, and feedback increased hepatic expression of low-density lipoprotein (LDL) receptor, which results in enhanced LDL-cholesterol clearance in the circulation. Because plasma LDL cholesterol level is strongly associated with coronary heart disease, it has been generally assumed that the beneficial effects underlying statin therapy are entirely due to cholesterol reduction. Interestingly, both experimental and clinical evidence reveal the overall beneficial effects of statins extend beyond those obtained by simply lowering serum cholesterol levels [4-6].