Copyright © 2006, European Society of Cardiology
Revisiting p53 and its effectors in ischemic heart injury
Johns Hopkins University School of Medicine, Department of Medicine, 5501 Hopkins Bayview Circle, Rm 5A.58, Baltimore, MD 21224, United States
* Tel.: +1 410 550 4148; fax: +1 410 550 2612. Email address: mcrow1@jhmi.edu
Received 6 April 2006; accepted 7 April 2006
| The first 150 words of the full text of this article appear below. |
See article by Matsusaka et al. [4] (pages 457–465) in this issue.
p53 is a tumor suppressor that enforces normal growth control and genomic stability. Its importance is reflected in the fact that acquired mutations in it or its upstream activators are found in all major human cancers [1]. p53 controls aberrant or inappropriate growth by acting as a transcription factor for a number of genes that promote apoptosis or growth arrest (Fig. 1). In addition, recent studies indicate that there are important non-transcriptional effects of p53 on apoptosis that involve its ability to suppress anti-apoptotic or activate pro-apoptotic Bcl-2 family members [2]. p53 expression or activity increases in cells in response to DNA damage and other forms of cell stress, including hypoxia [3], a major component of ischemic injury. Controversy over what role, if any, p53 plays in the response of the heart
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1. p53 and cardiomyocyte cell death in culture |
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2. In vivo veritas |
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3. Other recent studies |
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