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Cardiovascular Research Advance Access originally published online on November 20, 2007
Cardiovascular Research 2008 77(3):448-451; doi:10.1093/cvr/cvm074
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2007. For permissions please email: journals.permissions@oxfordjournals.org

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 in1], 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 to . . . [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
 

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