Skip Navigation


Cardiovascular Research Advance Access first published online on November 20, 2007
This version [Corrected Proof] published online on December 15, 2007
Cardiovascular Research, doi:10.1093/cvr/cvm074
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
77/3/448    most recent
cvm074v3
cvm074v2
cvm074v1
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 Sanchis, D.
Right arrow Articles by Comella, J. X.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sanchis, D.
Right arrow Articles by Comella, J. X.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

An alternative view of apoptosis in heart development and disease

Daniel Sanchis*, Marta Llovera, Manel Ballester and Joan X. Comella{dagger}

Cell Signaling and Apoptosis Group, Biomedical Research Institute of Lleida (IRBLLEIDA), Av. Rovira Roure, 80, 25198 Lleida Spain

* Corresponding author. Tel: +34 973702215; fax: +34 973702213. E-mail address: daniel.sanchis@cmb.udl.cat

The first 10% of the full text of this article appears below.

Although the involvement of caspases in cardiomyocyte death is widely accepted [reviewed in 1], increasing experimental evidence suggests that caspase activation is not relevant for post-mitotic cardiomyocyte cell death.2–7 Controversy also exists as to the mechanisms conferring cardioprotection by caspase inhibitors, which could be unrelated to apoptosis or target non-myocardial cells.8–11 In addition, the genes controlling the caspase-dependent death pathway are silenced during early post-natal development.7,12 Finally, the major role of death receptors and the Bcl-2-related proteins in the myocardium is probably to control differentiation, adaptation to stress and mitochondrial integrity. In light of these findings, we propose here an alternative explanation of the role of canonical apoptosis regulators in the control of cardiomyocyte life and death.


   1. Caspase-dependent signalling is important during heart morphogenesis and is later silenced in post-mitotic cardiomyocytes
 
Cell death implying apoptotic-like DNA damage occurs during embryonic heart development.13–15 Experiments using caspase inhibitors suggest that caspase-dependent cell death occurs in the cardiac regions submitted . . . [Full Text of this Article]


   2. Mitochondrial damage implicated in post-mitotic cardiomyocyte death is not associated with caspase activation
 

   3. Death receptor-dependent apoptosis is involved in non-myocyte cell death in experimental models of heart disease
 

   4. Death receptors play a relevant role in cardiomyocyte differentiation and growth
 

   5. Concluding remarks
 

   Funding
 

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