作者: R. Kleemann , T. Kooistra
DOI: 10.2174/156800605774962077
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摘要: Besides classical risk factors such as hypercholesterolemia and hypertension, chronic subacute inflammation has recently been recognized an important force driving the development of atherosclerosis, most common underlying cause myocardial infarction stroke. There is compelling evidence that a disturbance cholesterol homeostasis contributes to inflammatory state inhibitors HMG-CoA reductase (statins) may dampen inappropriate responses. We review suggest mechanisms by which dietary can induce atherogenic response in liver vessel wall, with particular emphasis on time course this during atherogenesis interplay between these tissues. discuss how statins interfere process, whether they reduce via a) their cholesterol-lowering effect, and/or b) cholesterol-independent (pleiotropic) vasculoprotective activities. Recent studies performed (humanized) animal models allow us distinguish lipid-lowering-dependent from lipid-lowering-independent functions statins. Using data, we degree effects contribute reduction inflammation, allowing estimation relevance pleiotropic statin for human situation.