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Cardiovascular Research 2001 52(1):5-7; doi:10.1016/S0008-6363(01)00418-7
© 2001 by European Society of Cardiology
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Copyright © 2001, European Society of Cardiology

Emerging mechanisms for secondary cardioprotective effects of statins

Steven J Miller*

Division of Experimental Pathology, Methodist Research Institute, Clarian Health Partners Inc. (Methodist, Indiana University, Riley Hospitals), 1701 N. Senate Blvd., Indianapolis, IN 46202, USA

smiller2@clarian.com

* Tel.: +1-317-929-1670; fax: +1-317-929-5954

Received 30 July 2001; accepted 31 July 2001

The first 10% of the full text of this article appears below.

See article by Li et al. [11] (pages 130–135) in this issue.


   1. Introduction
 
A widely accepted risk factor for the development of coronary artery disease is an elevated level of plasma cholesterol. Early on, it was recognized that inhibition of de novo synthesis of cholesterol could be an effective method to reduce plasma cholesterol, and thereby potentially reduce the incidence of atherosclerosis. The rate-limiting step in cholesterol synthesis is the reduction of 3-hydroxy-3-methylglutaryl (HMG)-CoA to mevalonate, which is catalyzed by HMG-CoA reductase. This enzyme is an obvious target for inhibition in order to bring about a reduction in cholesterol synthesis and a corresponding drop in plasma cholesterol. The first specific inhibitor of HMG-CoA reductase to be discovered was a fungal metabolite named compactin [1,2], closely followed by mevinolin [3,4]. Synthetic derivatives of these compounds, along with other naturally occurring compounds, have spawned a wide variety of . . . [Full Text of this Article]


   2. Pleiotropic effects of statins
 

   3. Regulation of LOX-1 receptor by statins
 

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