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Cardiovascular Research Advance Access first published online on September 8, 2008
This version [Corrected Proof] published online on September 29, 2008
Cardiovascular Research, doi:10.1093/cvr/cvn243
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org.

Apoptotic and non-apoptotic programmed cardiomyocyte death in ventricular remodelling

Gerald W. Dorn, II*

Center for Pharmacogenomics and Cardiovascular Division, Department of Internal Medicine, Washington University, 660 S. Euclid Ave., Campus Box 8086, St Louis, MO 63110, USA

* Corresponding author. Tel: +1 314 362 8901; fax: +1 314 362 0186. E-mail address: gdorn{at}dom.wustl.ed

A defining cellular event in the transition from compensated hypertrophy to dilated cardiomyopathy is cardiomyocyte drop-out due to apoptosis, programmed necrosis, and autophagy. The importance of apoptosis in heart failure has been recognized for over a decade, while other forms of programmed cell death have more recently been appreciated, and their pathophysiological roles continue to be defined in experimental and clinical heart failure. The major focus of this review is on apoptosis in heart failure, with a discussion of molecular cross-talk between apoptosis, autophagy, and programmed necrosis.

KEYWORDS Apoptosis; Autophagy; Necrosis; Mitochondria; Heart failure

Time for primary review: 17 days


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