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Heart 2000;84:355-356; doi:10.1136/heart.84.4.355
Copyright © 2000 BMJ Publishing Group Ltd & British Cardiovascular Society
Heart 2000;84:355-356 ( October )

Editorial

Apoptosis: a pivotal event or an epiphenomenon in the pathophysiology of heart failure?

The first 150 words of the full text of this article appear below.

Apoptosis, or programmed cell death, is an evolutionary conserved genetically programmed process by which multicellular organisms regulate cell numbers. It is critical in development and in tissue homeostasis. Unlike necrosis, the process is active, energy requiring and precisely regulated.

Apoptosis in cardiac development and disease

Cardiac myocytes are by and large terminally differentiated and have a limited capacity for self renewal. It would therefore seem that loss of a significant number of cardiomyocytes would have lasting adverse consequences. Apoptosis is, however, integral to normal cardiac development and is also important in the morphogenesis of the conducting system. This can be illustrated by accessory pathway mediated arrhythmias caused by inadequate removal of loop short circuit cells by apoptosis. Apoptotic cardiomyocytes have also been identified in subjects with ischaemic heart disease and myocarditis. Moreover, evidence exists to show that apoptosis occurs in "end stage" heart failure. The relevance of this process in . . . [Full text of this article]


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This article has been cited by other articles:

  • Monnet, E., Chachques, J. C. (2005). Animal Models of Heart Failure: What Is New?. Ann. Thorac. Surg. 79: 1445-1453 [Abstract] [Full Text]  
  • Cai, L., Li, W., Wang, G., Guo, L., Jiang, Y., Kang, Y. J. (2002). Hyperglycemia-Induced Apoptosis in Mouse Myocardium: Mitochondrial Cytochrome c-Mediated Caspase-3 Activation Pathway. Diabetes 51: 1938-1948 [Abstract] [Full Text]  

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