Apoptosis occurs normally both during development and throughout adulthood, and serves to remove unwanted, aged, or potentially harmful cells. It is also a pathologic event when diseased cells become damaged beyond repair and are eliminated.

Apoptosis in Physiologic Situations Death by apoptosis is a normal phenomenon that serves to eliminate cells that are no longer needed, and to maintain a steady number of various cell populations in tissues. It is important in the following physiologic situations:

• The destruction of cells during embryogenesis, including implantation, organogenesis, developmental involution, and metamorphosis. The term programmed cell death was originally coined to denote death of specific cell types that was precisely regulated and occurred at defined times during the development of multicellular organisms. Apoptosis is a generic term for this pattern of cell death, regardless of the context, but it is often used interchangeably with programmed cell death. However, it is best to avoid this term to denote apoptosis, since in some cases necrosis may also be a form of programmed cell death

• Involution of hormone-dependent tissues upon hormone withdrawal, such as endometrial cell breakdown during the menstrual cycle, ovarian follicular atresia in menopause, the regression of the lactating breast after weaning, and prostatic atrophy after castration.

• Cell loss in proliferating cell populations, such as immature lymphocytes in the bone marrow and thymus and B lymphocytes in germinal centers that fail to express useful antigen receptors, and epithelial cells in intestinal crypts, so as to maintain a constant number (homeostasis).

• Elimination of potentially harmful self-reactive lymphocytes, either before or after they have completed their maturation, so as to prevent reactions against one’s own tissues.

• Death of host cells that have served their useful purpose, such as neutrophils in an acute inflammatory response, and lymphocytes at the end of an immune response. In these situations cells undergo apoptosis because they are deprived of necessary survival signals, such as growth factors.

Apoptosis in Pathologic Conditions

Apoptosis eliminates cells that are injured beyond repair without eliciting a host reaction, thus limiting collateral tissue damage. Death by apoptosis is responsible for loss of cells in a variety of pathologic states:

• DNA damage. Radiation, cytotoxic anticancer drugs, and hypoxia can damage DNA, either directly or via production of free radicals. If repair mechanisms cannot cope with the injury, the cell triggers intrinsic mechanisms that induce apoptosis. In these situations elimination of the cell may be a better alternative than risking mutations in the damaged DNA, which may result in malignant transformation.

• Accumulation of misfolded proteins. Improperly folded proteins may arise because of mutations in the genes encoding these proteins or because of extrinsic factors, such as damage caused by free radicals. Excessive accumulation of these proteins in the ER leads to a condition called ER stress, which culminates in apoptotic cell death. Apoptosis caused by the accumulation of misfolded proteins has been invoked as the basis of several degenerative diseases of the central nervous system and other organs.

• Cell death in certain infections, particularly viral infections, in which loss of infected cells is largely due to apoptosis that may be induced by the virus (as in adenovirus and HIV infections) or by the host immune response (as in viral hepatitis). An important host response to viruses consists of cytotoxic T lymphocytes specific for viral proteins, which induce apoptosis of infected cells in an attempt to eliminate reservoirs of infection. During this process there can be significant tissue damage. The same T-cell–mediated mechanism is responsible for cell death in tumors and cellular rejection of transplants.

• Pathologic atrophy in parenchymal organs after duct obstruction, such as occurs in the pancreas, parotid gland, and kidney.

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مواضيع ذات صلة

Damage to DNA and Proteins

Morphologic and Biochemical Changes in Apoptosis

surgical site Infection

Ventilator-associated pneumonia

Catheter-related Bloodstream Infection (CRBSI)

Etiopathogenesis of Diabetes Mellitus

Classification of Diabetes Mellitus

Defects in Membrane Permeability

Accumulation of Oxygen-Derived Free Radicals(Oxidative Stress)

Influx of Calcium and Loss of Calcium Homeostasis

Endocrine Disorders of the Ovary

Mitochondrial Damage