title: Cross-talk between exogenous statins and endogenous high-density lipoprotein in anti-inflammatory and anti-atherogenic actions.
abstract: The reverse cholesterol transport mediated by high-density lipoprotein (HDL) is an important mechanism for maintaining body cholesterol at normal levels and, hence, the critical anti-atherogenic action of the lipoprotein. Recent studies, however, showed that HDL exerts a variety of anti-inflammatory and anti-atherogenic actions independently of the cholesterol metabolism. On the other hand, statins, inhibitors of HMG-CoA reductase, were initially developed to lower low-density lipoprotein cholesterol in plasma, and they are now recognized to exert a variety of pleiotropic or beneficial actions. Thus, although the mechanisms are different, both endogenous HDL and exogenous statins regulate cholesterol balance in a negative manner and exert a variety of beneficial actions independently of their cholesterol-lowering activity. These results raise the possibility that statins act in part through modulating the plasma levels of HDL and/or its actions. Here, we reviewed the cross-talk mechanism between statins and HDL in anti-inflammatory and anti-atherogenic actions, with a focus on scavenger receptor class B type I, one of main players involved in the cholesterol metabolism-independent HDL actions, and its downstream signaling pathway, leading to the activation of endothelial nitric oxide synthase and the inhibition of adhesion molecule expression in endothelial cells.
authors.affiliation: Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Japan.
authors.forename: Takao
authors.initials: T
authors.lastname: Kimura
authors.forename: Koichi
authors.initials: K
authors.lastname: Sato
authors.forename: Hideaki
authors.initials: H
authors.lastname: Tomura
authors.forename: Fumikazu
authors.initials: F
authors.lastname: Okajima
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D000924:Anticholesteremic Agents / Q000494:pharmacology*; D050197:Atherosclerosis / Q000517:prevention & control*; D018955:CD36 Antigens / Q000502:physiology; D002448:Cell Adhesion / Q000502:physiology; D002784:Cholesterol / Q000378:metabolism; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology; D025461:Feedback, Physiological / Q000187:drug effects*; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology*; D007962:Leukocytes / Q000502:physiology; D008075:Lipoproteins, HDL / Q000502:physiology*; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D049349:Receptors, Lysosphingolipid / Q000502:physiology; D020741:rho GTP-Binding Proteins / Q000502:physiology
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D000924:Anticholesteremic Agents; D018955:CD36 Antigens; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008075:Lipoproteins, HDL; D049349:Receptors, Lysosphingolipid; D002784:Cholesterol; D052250:Nitric Oxide Synthase Type III; D020741:rho GTP-Binding Proteins