This first installment of the two volume book on Programmed Cell Death provides a
series of concise review articles presenting our current understanding of the cascades
of events involved in apoptosis or programmed cell death and signaling pathways
that can be engaged to prevent apoptosis. The past five years have seen a virtual
explosion in the number of laboratories studying, at the molecular and cellular levels,
the mechanisms that lead to cell death of the form called apoptosis which manifests
specific morphological, biochemical, and molecular features that distinguish this form
of cell death from necrosis. The morphological features of cells undergoing apoptosis
include cell shrinkage, surface membrane blebbing, cytoskeletal perturbation, and
nuclear chromatin condensation and fragmentation. In addition, organellar structure,
(i.e. structure of mitochondria, endoplasmic reticulum, and golgi) are largely preserved
in cells undergoing apoptosis. Biochemical features of apoptosis include activation of
a class of cysteine proteases called caspases, mitochondrial membrane depolarization,
and release of factors, such as cytochrome c, that seem to be critical for nuclear
manifestations of apoptosis. In addition, a relatively stereotyped sequence of gene
and protein expression occurs involving upregulation of proteins involved in inducing
mitochondrial dysfunction and caspase activation, on the one hand, and anti-apoptotic
genes that may be involved in suppressing the apoptotic cascade, on the other hand.