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(Circulation. 2005;112:6-8.)
© 2005 American Heart Association, Inc.

Editorial

Cell Death and Adenosine Triphosphate

The Paradox

Jutta Schaper, MD, PhD; Sawa Kostin, MD

From the Department of Experimental Cardiology, Max-Planck-Institute, Bad Nauheim, Germany.

Correspondence to Jutta Schaper, MD, Max-Planck-Institute, Benekestrasse 2, D-61231 Bad Nauheim, Germany. E-mail jschaper@kerckhoff.mpg.de

Key Words: Editorials • apoptosis • necrosis • ischemia • proto-oncogene proteins c-bcl-2

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The inhibition of cell death lies at the heart of the interesting publication in this issue of Circulation by Huang et al.¹ The authors’ major message is that Bcl-xL gene transfer prolongs the cold preservation time of rat hearts destined for transplantation. Bcl-xL belongs to the large Bcl-2 family and has been reported to inhibit Bax translocation to the mitochondria and to reduce cytochrome c release, thereby interrupting the apoptotic cascade and reducing the number of cells dying by apoptosis.^2,3 This is precisely what Huang et al¹ have shown—namely, that inhibition of the apoptotic pathway can partially prevent the deleterious effects of long-term ischemia by reducing the rate of apoptosis. In addition, these authors show that "infarct size" was reduced in treated hearts and that the rate of polymorphonuclear cell infiltration was minimal as compared with hearts without gene transfer. Infarct size was determined in Langendorff buffer–perfused hearts without any coronary artery ligation and describes the tissue area with necrotic cells as demonstrated by triphenyltetrazolium (TTC) staining. To the uninitiated reader it appears, therefore, that an intervention aimed at reducing apoptosis is also able to interfere with the process of ischemic cell death, ie, with oncosis (this is the preferred, modern term for necrosis; necrosis proper is the process of cell demise after any type of cell death⁴). The number of cardiomyocytes dying by either cell death mechanism, apoptotic or oncotic, was reduced: Only 6.5% of all cardiomyocytes were terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) positive in . . . [Full Text of this Article]

Related Article:

Bcl-xL Gene Transfer Inhibits Bax Translocation and Prolongs Cardiac Cold Preservation Time in Rats

Jianhua Huang, Kiminori Nakamura, Yoshinori Ito, Takeshi Uzuka, Masayuki Morikawa, Sachie Hirai, Kei Tomihara, Toshihiro Tanaka, Yukari Masuta, Keiji Ishii, Kazunori Kato, and Hirofumi Hamada
Circulation 2005 112: 76-83. [Abstract] [Full Text]

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