Sandy Maumus-Robert

1 Introduction Statins are lipid-lowering drugs used to prevent cardiovascular diseases. They act by inhibiting the catalysis of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) into mevalonate by HMG CoA reductase, thus reducing cholesterol synthesis by the liver. Beside this effect on cholesterol reduction, statins reduce inflammation and oxidative stress and up-regulate endothelial NO-synthase activity, thereby improving endothelial functions and stabilizing the atherosclerotic plaque (1).

Anticancer drugs targeting angiogenesis act either directly on vascular endothelial growth factor (VEGF) receptors (VEGF inhibitors) or VEGF-mediated intracellular processes (tyrosine kinase inhibitors) or indirectly through downstream VEGF signaling within broader processes (mammalian target of rapamycin inhibitors and multiprotein kinase inhibitors).