Skip Navigation

Cardiovascular Research 2004 61(3):414-426; doi:10.1016/j.cardiores.2003.12.023
© 2004 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
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
Google Scholar
Right arrow Articles by Eefting, F.
Right arrow Articles by Doevendans, P. A
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Eefting, F.
Right arrow Articles by Doevendans, P. A
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2004, European Society of Cardiology

Role of apoptosis in reperfusion injury

Frank Eeftinga, Benno Rensinga, Jochem Wigmana, Willem Jan Pannekoeka, Wai Ming Liua, Maarten Jan Cramera, Daniel J Lipsa and Pieter A Doevendans*,a,b

aDepartment of Cardiology, Heart Lung Center Utrecht, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands
bInteruniversity Cardiology Institute the Netherlands, The Netherlands

* Corresponding author. Department of Cardiology, Heart Lung Center Utrecht, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands. Tel.: +31-30-2509111; fax: +31-30-2542155. p.doevendans{at}azu.nl

Many changes occur during reperfusion of the myocardium after ischemic damage. Necrosis and apoptosis appear to be ongoing during ischemia, while apoptosis is boosted by the reperfusion event. In the past 10 years, distinct intracellular pathways important for hypertrophy, apoptosis, cardiac failure, ischemic preconditioning and reperfusion damage have been recognized. The eventual response of the cardiomyocyte will depend on energy and time available as well as changes in pH and ion handling and the delicate balance of activation of signaling molecules and transcription factors. There is agreement on the central role of mitochondria and nitric oxide (NO) in programmed cell death. However, although many groups analyzed the contribution of NO to cell death, still the circumstances and levels required for cardioprotection or death are unclear. Growth factors, cytokines, and downstream signaling molecules have been shown to influence programmed cell death through mechanisms reminiscent of preconditioning. Here, the role of apoptosis in ischemia reperfusion-related cell death is reviewed. Important data have been obtained in isolated cells, intact hearts and intact animals. Both pharmacological as well as genetic interventions are discussed. Proof for apoptosis in man post-myocardial infarction (MI) treated through primary Percutaneous Trans-luminal Coronary Angioplasty or other reperfusion therapy is reviewed. Finally, the currently available quantification methods for apoptosis post-MI are mentioned.

KEYWORDS Apoptosis; Caspase blockers; Reperfusion injury; Cardiomyocyte; Mitochondria; Nitric oxide; Growth factors; Annexin-V

Time for primary review 23 days


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


This article has been cited by other articles:


Home page
 Anesth. Analg.Home page
P. S. Pagel
Induction of Heat Shock Protein 70 and Preconditioning by Sevoflurane: A Potent Protective Interaction Against Myocardial Ischemia-Reperfusion Injury
Anesth. Analg., September 1, 2008; 107(3): 742 - 745.
[Full Text] [PDF]

Home page
 Anesth. Analg.Home page
P. S. Pagel, J. G. Krolikowski, P. F. Pratt Jr, Y. H. Shim, J. Amour, D. C. Warltier, and D. Weihrauch
The Mechanism of Helium-Induced Preconditioning: A Direct Role for Nitric Oxide in Rabbits
Anesth. Analg., September 1, 2008; 107(3): 762 - 768.
[Abstract] [Full Text] [PDF]


Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.