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HAX-1 represses postmitochondrial caspase-9 activation and cell death during hypoxia-reoxygenation.

See related article, pages 415–423 

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 previously1–3). The cleavage of caspase-specific substrates results in the biochemical destruction of the cell and phenotypic changes associated with apoptosis. To date, more than 14 caspases have been identified (reviewed previously2,3). Of these, caspase-2, -8, -9, and -10 are thought to be initiator caspases, whereas caspase-3, -6, and -7 are considered to be death effectors. Other caspases, including caspase-1, -4, -5, -11, -13, and -14, …