Abstract

The 3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase inhibitors (statins) are a class of drug used to lower low-density lipoprotein (LDL) levels. However, in recent years, statins have been shown to possess a pleiotropic effect beyond its cholesterol lowering ability, including attenuating the effect of ischaemia reperfusion injury. This review considers the biomolecular processes that may lead to this beneficial effect.

Keywords: Ischaemia reperfusion injury, statins, 3-hydroxy-3-methyl-glutaryl-CoA, reductase inhibitors, low-density lipoprotein, inflammatory re-sponse syndrome, multi organs dysfunction syn-drome, tissue hypoxia, hypoxanthine, xanthine oxidase, reactive oxygen species, nuclear factor B, activator protein-1, nitric oxide, endothelial dysfunction, inter-leukin (IL)-1, tumour necrosis factor alpha, platelet-activating factor, sialyl Lewis X, thrombin, cytokines, vascular endothelial cadherin, angioplasty, cholesterol biosynthesis, lovastatin, pravastatin, simvastatin, atorvastatin, cerivastatin, fluvastatin, rosuvastatin, cytochrome P450, coronary heart disease, rhabdo-myolysis, endothelial NO synthase, inducible NO synthase, neuronal NO synthase, Pro-Inflammatory Cytokines, PAF receptor, endothelin-1, monocyte chemoattractant protein-1, thrombomodulin, cytokine transcription, C-reactive protein, Leukocytes-Endothelial Interaction, decay-accelerating factor, protein kinase C, NADPH-oxidase, ROS reduction