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(Circulation. 2002;106:2640.)
© 2002 American Heart Association, Inc.

Editorial

E2F1

A Magic Bullet for Atherosclerosis?

Chunming Dong, MD; Pascal J. Goldschmidt-Clermont, MD

From the Division of Cardiology, Department of Medicine, Duke University Medical Center, Durham, NC.

Correspondence to Chunming Dong, Division of Cardiology, Department of Medicine, Duke University Medical Center, Box 3444, Durham, NC 27710. E-mail dong0005@mc.duke.edu

Key Words: Editorials • atherosclerosis • inflammation • signal transduction

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The E2F family of transcription factors (E2Fs) plays an important role in the regulation of cell proliferation and apoptosis and includes 6 structurally related E2F proteins (E2F1 through 6). E2Fs function as heterodimers with members of the DP family (DP-1 and DP-2) to transactivate or repress gene expression and play important roles in regulating both cell proliferation and antiproliferative processes such as apoptosis and senescence.¹ Atherosclerosis represents a defective reparative process in response to repeated injuries to the vessel wall.² Central to the resulting inflammatory reaction are proinflammatory cytokines, bacterial and viral products, and reactive oxygen intermediates, all of which activate nuclear factor kappa-B (NFB), which controls the transcription of over 100 genes that encode mediators of innate immune and inflammatory responses.³ Among these induced genes are leukocyte adhesion molecules, metalloproteinases (MMPs), and proinflammatory cytokines, including tumor necrosis factor- (TNF) and interleukin-6 (IL-6), which, in turn, can activate NFB.⁴ Hence, NFB not only promotes the recruitment and activation of inflammatory cells, but also serves as a central switch within a positive feedback loop that regulates the expression of proinflammatory factors in the development of atherosclerosis. In addition, NFB works in concert with other transcription factors, activator protein-1 (AP-1) in particular, to activate the expression of pro-atherosclerotic genes⁵. In this context, atherosclerosis can be viewed as an inflammatory process that is critically dependent on the transcriptional activation of cytokine genes under the control of NFB and other transcription factors.

See p 2707

The relevance . . . [Full Text of this Article]

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E2F-1 Regulates Nuclear Factor-B Activity and Cell Adhesion: Potential Antiinflammatory Activity of the Transcription Factor E2F-1

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Circulation 2002 106: 2707-2713. [Abstract] [Full Text]

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