ISSN: 2044-9038 (Print) 2044-9046 (Electronic)

Clinical Practice

Apoptosis Open Access Articles

Apoptosis, known as programmed cell death, is a carefully controlled, energy-dependent process of cell death. Induction of apoptosis results in a cascade of characteristic biochemical events resulting in changes in cellular morphology and death. Cells undergoing apoptosis display blebbing, cell shrinkage, nuclear fragmentation, and DNA fragmentation. In contrast to necrosis, apoptotic cells form apoptotic bodies that are phagocytized by neighboring cells, without the release of cellular contents. Apoptosis plays important roles in physiology and pathology, and can be triggered by numerous stimuli, including ischemia, hypoxia, exposure to certain drugs and chemicals, immune reactions, infectious agents, high temperature, radiation, and various disease states. Apoptosis plays a critical role during normal development and homeostasis of adult tissues. Consequently, deregulation of apoptosis is commonly associated with diseases ranging from cancer to neurodegeneration. Toxicants also induce cell death via apoptosis, and in most cases this involves the activation of cysteinyl aspartate-specific proteases (caspases). In this chapter, we describe in biochemical and structural detail the mechanisms that mediate the activation of caspases within large multimeric complexes, including the death-inducing signaling complex (DISC) and the Apaf-1 apoptosome. In addition, we cover each of the factors known to directly or indirectly regulate the activation (or activity) of caspases, including inhibitor of apoptosis (IAP) and BCL-2 family members, as well as their antagonists.    

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