This Article Full Text Full Text (PDF) All Versions of this Article: 26/3/449    most recent 01.ATV.0000196747.79349.d1v1 Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ichiki, T. Search for Related Content PubMed PubMed Citation Articles by Ichiki, T.

(Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:449.)
© 2006 American Heart Association, Inc.

Brief Reviews

Role of cAMP Response Element Binding Protein in Cardiovascular Remodeling

Good, Bad, or Both?

Toshihiro Ichiki

From the Department of Cardiovascular Medicine, Kyushu University Graduate School of Medical Sciences, Higashi-ku, Fukuoka, Japan.

Correspondence to Toshihiro Ichiki, Department of Cardiovascular Medicine, Kyushu University Graduate School of Medical Sciences, 3-1-1 Maidashi, Higashi-ku, 812-8582 Fukuoka, Japan. E-mail ichiki{at}cardiol.med.kyushu-u.ac.jp

The cAMP response element binding protein (CREB) is a ubiquitously expressed nuclear transcription factor that is activated by various extracellular stimuli. CREB is known to regulate the expression of genes important to cell proliferation, differentiation, adaptation, and survival in many cell types. Loss of CREB function by transgenic overexpression of dominant negative CREB or targeted deletion of the CREB gene revealed that CREB is involved in the differentiation of T lymphocytes, production of growth hormone, and the long-term potentiation of neuronal memory. The role of CREB in cardiovascular system is incompletely characterized and several controversies remain. A growing body of recent evidence, however, has suggested that CREB plays an important role in the cardiovascular remodeling process, including inflammation, cell migration, and apoptosis. Thus, CREB may be a possible target for the treatment of cardiovascular diseases such as atherosclerosis, restenosis, and reperfusion injury.

The cAMP response element binding protein (CREB) is a nuclear transcription factor activated by various extracellular stimuli. The role of CREB in cardiovascular system is incompletely characterized and several controversies remain. A growing body of recent evidence, however, has suggested that CREB plays an important role in the cardiovascular remodeling.

Key Words: cAMP response element binding protein • gene transcription • protein kinase • signal transduction

This article has been cited by other articles:

				G. Nino, A. Hu, J. S. Grunstein, and M. M. Grunstein Mechanism regulating proasthmatic effects of prolonged homologous {beta}2-adrenergic receptor desensitization in airway smooth muscle Am J Physiol Lung Cell Mol Physiol, October 1, 2009; 297(4): L746 - L757. [Abstract] [Full Text] [PDF]

				Y. C. Chan and P. S. Leung Involvement of Redox-Sensitive Extracellular-Regulated Kinases in Angiotensin II-Induced Interleukin-6 Expression in Pancreatic Acinar Cells J. Pharmacol. Exp. Ther., May 1, 2009; 329(2): 450 - 458. [Abstract] [Full Text] [PDF]

				Q. Lu, B. Patel, E. O. Harrington, and S. Rounds Transforming growth factor-{beta}1 causes pulmonary microvascular endothelial cell apoptosis via ALK5 Am J Physiol Lung Cell Mol Physiol, May 1, 2009; 296(5): L825 - L838. [Abstract] [Full Text] [PDF]

				D. J. Samuvel, K. P. Sundararaj, A. Nareika, M. F. Lopes-Virella, and Y. Huang Lactate Boosts TLR4 Signaling and NF-{kappa}B Pathway-Mediated Gene Transcription in Macrophages via Monocarboxylate Transporters and MD-2 Up-Regulation J. Immunol., February 15, 2009; 182(4): 2476 - 2484. [Abstract] [Full Text] [PDF]

				A. Hu, G. Nino, J. S. Grunstein, S. Fatma, and M. M. Grunstein Prolonged heterologous {beta}2-adrenoceptor desensitization promotes proasthmatic airway smooth muscle function via PKA/ERK1/2-mediated phosphodiesterase-4 induction Am J Physiol Lung Cell Mol Physiol, June 1, 2008; 294(6): L1055 - L1067. [Abstract] [Full Text] [PDF]

				R. Tan, X. Zhang, J. Yang, Y. Li, and Y. Liu Molecular Basis for the Cell Type Specific Induction of SnoN Expression by Hepatocyte Growth Factor J. Am. Soc. Nephrol., August 1, 2007; 18(8): 2340 - 2349. [Abstract] [Full Text] [PDF]

				P. A. Sonalker and E. K. Jackson Norepinephrine, via {beta}-Adrenoceptors, Regulates Bumetanide-Sensitive Cotransporter Type 1 Expression in Thick Ascending Limb Cells Hypertension, June 1, 2007; 49(6): 1351 - 1357. [Abstract] [Full Text] [PDF]

				U. Singh, S. Devaraj, M. R. Dasu, D. Ciobanu, J. Reusch, and I. Jialal C-Reactive Protein Decreases Interleukin-10 Secretion in Activated Human Monocyte-Derived Macrophages via Inhibition of Cyclic AMP Production Arterioscler Thromb Vasc Biol, November 1, 2006; 26(11): 2469 - 2475. [Abstract] [Full Text] [PDF]