Pleiotropic effects of HMG-CoA reductase inhibitors.

摘要: Abstract HMG-CoA reductase, in addition to being the rate-limiting enzyme cholesterol biosynthetic pathway, is involved regulation of receptors for low-density lipoprotein (LDL)-cholesterol. Clinical studies men and women demonstrate that inhibitors reductase (statins), by reducing plasma cholesterol, may limit development atherosclerosis reduce risk mortality ischemic events. Preclinical evidence suggests under controlled conditions lowering, statins have ancillary properties or pleiotropic effects, which directly progression. In this review, effects been defined as 'ancillary statins, result hepatic and/or vascular changes not be a consequence inhibition reductase.' Beyond LDL lowering activity improvements noted endothelial dysfunction through direct stimulation expression such vasodilators nitric oxide reduction vasoconstrictors. Factors associated with atherogenesis, monocyte adhesion cells, macrophage production proinflammatory molecules matrix metalloproteases, smooth muscle cell proliferation migration macrophage-induced oxidation particles also reduced various statins. It unclear whether observed are independent LDL-cholesterol they clinically relevant; however, one can conclude appear class effect attenuated post-reductase product, mevalonate.