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(Circulation Research. 2008;103:331.)
© 2008 American Heart Association, Inc.

Editorials

ATF-4 and Vascular Injury

Integration of Growth Factor Signaling and the Cellular Stress Response

Michael T. Chin

From the Department of Medicine, Division of Cardiology, Center for Cardiovascular Biology, University of Washington, Seattle.

Correspondence to Michael T. Chin, Center for Cardiovascular Biology, University of Washington, 815 Mercer St, Rm 353, Seattle, WA 98109. E-mail mtchin@u.washington.edu

See related article, pages 378–387

Key Words: ATF-4 • vascular injury • FGF-2 • VEGF • smooth muscle proliferation

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

Smooth muscle proliferation and neointimal formation are characteristic features of vascular lesions that develop after vascular injury and contribute to the development of occlusive vascular lesions after percutaneous coronary interventions and in transplant vasculopathy. The traditional model for the development of these vascular lesions has postulated that a complex interplay among locally released growth factors and cytokines, circulating platelets and inflammatory cells, local smooth muscle and endothelial cells, and perhaps circulating precursor cells involving multiple cellular processes such as adhesion, proliferation, migration, and apoptosis is orchestrated at many levels, resulting in vascular stenosis. The temporal and spatial complexity of the overall process and the diverse contributions of various components have provided many opportunities for study, but identifying and linking the various critical steps in the development of occlusive vascular lesions has remained challenging. Although numerous studies examining roles of vascular signaling pathways and vascular transcription factors have been published, a clear picture of how signaling and transcription are intertwined remains elusive. In this issue of Circulation Research, Malabanan et al present a comprehensive series of experiments linking the transcription factor activating transcription factor (ATF)-4 to intimal thickening after injury and identify both upstream and downstream associated growth factor pathways, thereby providing additional insight into the orchestrated activation of transcriptional and signaling pathways in vascular disease.¹

The authors initially identified ATF-4 as a potential regulator of neointimal formation through a microarray screen for genes induced in smooth muscle cells (SMCs) by fibroblast growth factor (FGF)-2. FGF-2 has been identified previously . . . [Full Text of this Article]

Related Article:

Activation Transcription Factor-4 Induced by Fibroblast Growth Factor-2 Regulates Vascular Endothelial Growth Factor-A Transcription in Vascular Smooth Muscle Cells and Mediates Intimal Thickening in Rat Arteries Following Balloon Injury

Kristine P. Malabanan, Peter Kanellakis, Alexander Bobik, and Levon M. Khachigian
Circ. Res. 2008 103: 378-387. [Abstract] [Full Text] [PDF]

This article has been cited by other articles:

				S. F. Abcouwer and C. N. Roybal Regulation of Vascular Endothelial Growth Factor A by Activating Transcription Factor 4 Circ. Res., October 24, 2008; 103(9): e118 - e118. [Full Text] [PDF]

				L. M. Khachigian, A. Bobik, P. Kanellakis, and K. Malabanan Response to Abcouwer and Roybal Circ. Res., October 24, 2008; 103(9): e119 - e119. [Full Text] [PDF]