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First published online October 10, 2007

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Atherogenesis: cholesterol quashes TGF-

High levels of cholesterol are a major risk factor for atherosclerosis and, consequently, heart attacks and strokes. But how does cholesterol affect atherogenesis? Partly, report Jung San Huang and co-workers, by suppressing the responsiveness of vascular cells to the anti-atherosclerotic molecule transforming growth factor (TGF-; see p. 3509). TGF- antagonizes many key atherogenic events (for example, inflammation of blood vessel walls); so modulating responsiveness to TGF- is likely to affect the development of atherosclerosis. The authors show that cholesterol treatment suppresses TGF--induced signalling in several cell types, including endothelial cells. It does this, they report, by increasing the accumulation of TGF- receptors in lipid microdomains and facilitating the degradation of TGF-. By contrast, agents that lower or deplete cholesterol promote TGF--induced signalling. Finally, the authors show that TGF- responsiveness is suppressed in the aortic endothelium of atherosclerosis-prone mice fed a cholesterol-rich diet. These new insights into how cholesterol contributes to atherogenesis could lead to the development of new strategies for the treatment and prevention of atherosclerosis.

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Related articles in JCS:

Cholesterol suppresses cellular TGF- responsiveness: implications in atherogenesis

Chun-Lin Chen, I-Hua Liu, Steven J. Fliesler, Xianlin Han, Shuan Shian Huang, and Jung San Huang
JCS 2007 120: 3509-3521. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?