Programmed cell death; deletion of individual cells by fragmentation into membrane-bound particles, which are phagocytized by other cells. Syn: programmed cell death.
Whereas some cells (e.g., cardiac and skeletal muscle fibers, CNS neurons) last a lifetime, others (e.g., epithelial and glandular cells, erythrocytes) have limited life-spans, at the end of which they are genetically programmed for self-destruction by apoptosis, usually to be replaced by others formed by mitosis from surviving cells. Apoptosis also plays an essential role in morphogenesis and tissue homeostasis by eliminating transitory organs and tissues (e.g., pronephros and mesonephros) and cells formed in excess of bodily needs during embryogenesis, as well as cells that have been damaged or virally infected. Cells in tissue cultures spontaneously undergo apoptosis after about 50 cell divisions. In contrast to cell death caused by injury, infection, or circulatory impairment, apoptosis elicits no inflammatory response in adjacent cells and tissues. Features of apoptosis detectable by histologic and histochemical methods include cell shrinkage, due chiefly to dehydration; increased membrane permeability, with a rise in intracellular calcium and a fall in pH; nuclear and cytoplasmic condensation; endolytic cleavage of nuclear DNA into oligonucleosomal fragments; and ultimately formation of apoptotic bodies, which are absorbed and removed by macrophages. Besides being due to genetic programming, apoptosis can be induced by injury to cellular DNA, as by irradiation and some cytotoxic agents used to treat cancer. It can be suppressed by naturally occurring factors (e.g., cytokines) and by some drugs (e.g., protease inhibitors). Apoptosis typically does not occur in malignant cells. Such cells therefore escape the destiny of their nonmalignant precursor cells and are said to be immortal. Immortalization can occur in various ways. The BCL2 gene, present in many cancers, directs the production of an enzyme that blocks apoptosis and immortalizes affected cells. Injury to DNA normally triggers apoptosis by activating the p53 tumor suppressor gene, which is missing or mutated in about one half of all human cancers. Cells that lack this gene can survive chemotherapy and irradiation intended to destroy cancer cells. Failure of apoptosis to occur is also involved in some degenerative diseases, including lupus erythematosus, and may be responsible for cellular damage caused by certain viruses, including HIV. Apoptosis has thus far been observed only in animal cells.
Reference: Stedman's Medical Dictionary