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Postmitochondrial regulation of apoptosis during heart failure.

The biochemical basis for most of the morphological changes associated with apoptosis can be traced directly or indirectly to the actions of caspases, a family of intracellular cysteine proteases that function as effectors of programmed cell death (1, 2). Much of the recent progress toward mapping pathways for caspase activation has come from evaluations of normal dividing cells or established tumor lines, where obtaining large numbers of cells for biochemical analysis or transferring genes for functional analysis is readily possible. But, do all types of animal cells contain the same wiring instructions when it comes to connecting steps in cell suicide pathways? Researchers studying cell death in the heart are beginning to probe this question, and they are finding some surprises.