ABSTRACT

The effect of regulation of proliferation on cellular homeostasis has been studied for many years; the importance, however, of the converse phenomenon of programmed cell death (apoptosis) has only recently been recognized. The two ways in which cells may die are apoptosis and necrosis. Necrosis can be induced by cell injury caused by such diverse means as hyperthermia, hypoxia, complement attack, chemical treatment, toxins, or radiation. The release of cellular contents from necrotic cells into the extracellular fluid leads to tissue inflammation. Neutrophils undergo apoptotic cell death at the end of the inflammatory response and are phagocytosed by macrophages. Cells undergoing apoptosis display certain biochemical and physiological characteristics which differ from those shown by necrotic cells. Active macromolecular synthesis is required for induction of apoptosis in many cell types in response to most stimuli. Future research on apoptosis will likely involve elucidation of the signal transduction pathways involved in activation of the nuclease(s) responsible for internucleosomal DNA cleavage.