Skip Navigation

Cardiovascular Research 2006 70(3):401-403; doi:10.1016/j.cardiores.2006.04.003
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Crow, M. T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Crow, M. T.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2006, European Society of Cardiology

Revisiting p53 and its effectors in ischemic heart injury

Michael T. Crow*

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 . . . [Full Text of this Article]


   1. p53 and cardiomyocyte cell death in culture
 

   2. In vivo veritas
 

   3. Other recent studies
 

Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?