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Figure 1 Statin therapy may represent a potentially novel treatment strategy for preventing cardiac hypertrophy and for improving myocardial vascularization. Statins may exert beneficial effects in heart failure independent of cholesterol lowering by prevention of isoprenylation of small g proteins, such as Rac-1 or Rho-A, which have been shown to be critically involved in the activation of the oxidant enzyme NAD(P)H oxidase and the regulation of endothelial nitric oxide (NO) synthase expression. Prevention of NAD(P)H oxidase activation and an increased endothelial NO synthase-dependent NO availability may reduce cardiomyocyte hypertrophy and improve vascular (i.e., endothelial) function.
