NDLI: Activation transcription factor-4 and the acute vascular response to injury

Content Provider	Springer Nature Link
Author	Malabanan, Kristine P. Khachigian, Levon M.
Copyright Year	2010
Abstract	Atherosclerosis is a complex fibroproliferative–inflammatory process triggered by vascular injury. Transcription factors play an important role in the control of genes that effect critical changes in the vessel wall. Recent evidence indicates an emerging role for activation transcription factor 4 (ATF4), a master regulator for evolutionarily conserved mammalian stress response pathways, in cardiovascular pathologic settings. For example, in endothelial cells, ATF4 is induced by atherogenic factors such as oxidised phospholipids and homocysteine, and in monocytes, ATF4 is activated by hypoxia. In this context, ATF4 is thought to regulate pro-inflammatory signalling cascades and subsequent apoptosis. ATF4 is induced in aortic smooth muscle cells by fibroblast growth factor 2 and in the intact vessel wall following balloon angioplasty. Our own work indicates that ATF4 knockdown blocks injury-inducible intimal proliferation. Furthermore, studies in ATF4-deficient mice have established a role for ATF4 in diet-induced diabetes and hyperlipidaemia. In this article, we will review recent developments on the regulation of this intriguing nuclear protein and its transcriptional roles in the context of vascular injury and related disease.
Starting Page	545
Ending Page	552
Page Count	8
File Format	PDF
ISSN	09462716
Journal	Journal of Molecular Medicine
Volume Number	88
Issue Number	6
e-ISSN	14321440
Language	English
Publisher	Springer-Verlag
Publisher Date	2010-03-21
Publisher Place	Berlin/Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Transcription Cardiovascular disease Vascular biology ATF4 Vascular injury Atherosclerosis Restenosis Transcription factor Internal Medicine Human Genetics Molecular Medicine
Content Type	Text
Resource Type	Article
Subject	Drug Discovery Molecular Medicine Genetics (clinical)

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