Hmg-Coa Reductase Inhibitors
HMG-CoA reductase inhibitors (statins) are established drugs for the treatment of hypercholesterolemia. Furthermore, they induce regression of vascular atherosclerosis as well as reduction of cardiovascular-related morbidity and death in patients with and without coronary artery disease. This book deals with statins which have substantially altered the approach to therapy of atherosclerosis and its sequelae. Emphasis is placed on the scientific background to the discoveries and the development of the therapy, including an overview of the current state of knowledge of the drugs. Clinical data are reviewed extensively. This book not only provides the reader with valuable information but also stimulates further research into the pathogenesis of atherosclerosis and the mechanisms behind the action of effective statins. It sets the stage for creative thinking among scientists of many disciplines for the accomplishment of our ultimate goals in treating atherosclerosis and its sequelae. This topical volume...
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Na običajnih mestih nismo našli nobenih recenzij.
History and development of HMGCoA reductase inhibitors
Structure and mechanisms of action of HMGCoA reductase inhibitors
generegulatory target of statin action
Cellular effects of HMGCoA reductase inhibitors on blood cells monocytes macrophages platelets
Pleiotropic effects of HMGCoA reductase inhibitors on cells of the vascular wall
Druge izdaje - Prikaži vse
acid activity acute addition analysis apoB artery associated atherosclerosis atorvastatin binding Biol Chem blood Brown Cardiol cardiovascular cells cellular changes cholesterol levels cholesterol synthesis Circulation clinical compared concentrations coronary coronary events coronary heart disease cost cost-effectiveness death decreased diabetes differentiation disease domain drug effects of statins element element-binding endothelial Engl enzyme expression factors familial function gene glucose Goldstein JL HMG-CoA reductase inhibitors HMGR hs-CRP human hypercholesterolemia increase indicate inhibition involved LDL cholesterol lesion lipid lipoprotein liver lovastatin lowering macrophages mechanisms mediated mevalonate mmol/l monocytes mortality myocardial infarction observed oxide patients placebo plaque plasma platelet pravastatin prevention primary prevention production promoter protein receptor reduced regulation response risk role secondary secretion serum simvastatin SREBPs statin therapy sterol regulatory stroke subjects suggesting therapy Thromb tion transcription treatment trial vascular VLDL