Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Sci. STKE, 21 October 2003
Vol. 2003, Issue 205, p. tw417
[DOI: 10.1126/scisignal.2052003tw417]

EDITORS' CHOICE

CARDIOVASCULAR DISEASE Lipids and Pathogenesis

In coronary disease, accumulation of lipids along blood vessel walls progresses into characteristic lesions that are hallmarks of the disease process. Lee et al. (see the Perspective by Plutzky) show that the inflammatory response associated with atherogenesis may hinge on a nuclear receptor called PPAR{delta} that is expressed in macrophages. PPAR{delta} appears to control the expression of proinflammatory genes in mouse macrophages, and its absence in mice caused a reduction in lesions by about 60%. This nuclear receptor may thus act as a molecular switch of the inflammatory program in macrophages and may represent a key target point for controlling disease progression.

C.-H. Lee, A. Chawla, N. Urbiztondo, D. Liao, W. A. Boisvert, R. M. Evans, Transcriptional repression of atherogenic inflammation: Modulation by PPAR{delta}. Science 302, 453-457 (2003). [Abstract] [Full Text]

J. Plutzky, PPARs as therapeutic targets: Reverse cardiology? Science 302, 406-407 (2003). [Summary] [Full Text]

Citation: Lipids and Pathogenesis. Sci. STKE 2003, tw417 (2003).

To Advertise     Find Products

Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882