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(Circulation Research. 2006;99:336.)
© 2006 American Heart Association, Inc.

Editorials

HAX-1 Represses Postmitochondrial Caspase-9 Activation and Cell Death During Hypoxia–Reoxygenation

James Shaw, Lorrie A. Kirshenbaum

From The Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Departments of Physiology, Pharmacology & Therapeutics, Faculty of Medicine University of Manitoba, Winnipeg, Canada.

Correspondence to Dr Lorrie A. Kirshenbaum, Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Rm 3016, 351 Taché Ave, Winnipeg, Manitoba R2H 2A6, Canada. E-mail Lorrie@sbrc.ca

See related article, pages 415–423

Key Words: apoptosis • Hax-1 • mitochondria • caspases • ventricular myocytes • hypoxia

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

A delicate balance exists between cell growth and cell death. In the context of the adult myocardium, inappropriate or inordinate cell loss through an apoptotic process, coupled with the limited regenerative ability of the heart to repair after injury, has been suggested to be a contributing factor to the decline in ventricular performance in patients with heart failure. The ability to prevent or modulate untimely or inordinate cardiac cell death after myocardial injury would be of significant therapeutic value in maintaining cardiac function. For this reason, there has been considerable interest in deciphering the signaling pathways and cellular factors that govern cell survival and cell death under normal and disease conditions. Apoptosis has received considerable attention in recent years by virtue of the events leading to cell death occurring through a highly ordered, genetically regulated process. This lends versatility for the design of novel therapies against cellular targets known to activate or repress cell death.

Regulation of apoptosis in mammalian cells arises from the seminal discoveries of the ced-3, ced-4, and ced-9 genes in Caenorhabditis elegans. Mammalian counterparts to ced-3 and ced-4 have been cloned and identified. Ced-3 belongs to a large family of cellular cystine proteases, known collectively as caspases (for cysteinyl-aspartate–specific proteases) for their preferential ability to cleave cellular substrates after aspartic acid residues (reviewed previously^1–3). The cleavage of caspase-specific substrates results in the biochemical destruction of the cell and phenotypic changes associated with apoptosis. To . . . [Full Text of this Article]

Related Article:

Overexpression of HAX-1 Protects Cardiac Myocytes From Apoptosis Through Caspase-9 Inhibition

Yuchi Han, Yee-Shiuan Chen, Zhilin Liu, Natalya Bodyak, Debra Rigor, Egbert Bisping, William T. Pu, and Peter M. Kang
Circ. Res. 2006 99: 415-423. [Abstract] [Full Text] [PDF]

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