© 2004 by European Society of Cardiology
Copyright © 2004, European Society of Cardiology
Role of apoptosis in reperfusion injury
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
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