Can ACAT inhibition limit the progression of atherosclerosis in patients with coronary artery disease?
Jean-Claude Tardif* and Therese Heinonen
Correspondence *Montreal Heart Institute, 5000 Belanger Street, Montreal, QC H1T 1C8, Canada
Email jean-claude.tardif@icm-mhi.org
This article has no abstract so we have provided the first paragraph of the full text.
Current lipid-lowering therapies can reduce cardiovascular event rates by approximately a third. This reduction highlights their effectiveness; however, considering that the majority of events are not prevented, it also highlights the medical needs that remain. Inhibition of the enzyme ACAT, leading to reduced cholesterol esterification, has been a promising therapeutic target for atherosclerosis prevention. Indeed, inhibition of the ubiquitous ACAT1 could, in theory, prevent the transformation of macrophages into foam cells in the arterial wall, and inhibition of ACAT2 found in the liver and intestine could reduce serum lipids levels.1 Demonstration of the effect of ACAT inhibitors on both lipid lowering and reduction of plaque burden in animal models provided hope that these results would translate to clinical trials.
Full text of this article is available with one of the following:
- Personal subscription Purchase your own personal subscription to this journal. Already a subscriber? Please log in for immediate access.
- 7 day single article pass for US$18 In order to purchase this article you must be a registered user. Please register or log in.
- Site licence Learn more about institutional site licences
Current Subscribers
Please log in to access the full text article using the login box at the top of the page.
MORE ARTICLES LIKE THIS
These links to content published by NPG are automatically generated.
NEWS AND VIEWS
Cholesterol esters and atherosclerosis?a game of ACAT and mouseNature Medicine News and Views (01 Dec 2000)
