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Apoptosis

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Brain Injury

Abstract

Apoptosis, or programmed cell death, is a complex and strictly regulated cellular event. A prerequisite for apoptosis is the existence of highly conserved death programs within the cell genome. The induction of apoptosis is triggered by various intrinsic or extrinsic death signals. In brain these include, excitatory amino acids (EAA), calcium fluxes, free radicals, release of apoptogenic factors from damaged mitochondrion, binding of ligands to corresponding cell surface death receptors, lipid signaling molecules, and other toxins. Moreover, apoptosis can also be triggered by the loss of survival signals. Once initiated, organized cascades consisting of intracellular proenzymes, coenzymes, scaffold and chaperon proteins, and related molecules are set into motion. These pathways converge to a committed point, whereupon effector enzymes are activated that simultaneously lead to cytoskeletal disintegration, nuclear condensation, and digestion of DNA. Finally, the engulfment of the dead cell or cell fragments by phagocytosis peacefully terminates the death program. Incomplete execution of programmed cell death may redirect the cell to necrosis, which is an unfavorable event for the organism as a whole. Integrated cell death programs have been detected in all multi-cellular and unicellular organisms, including bacteria, and have been characterized in cell culture and in vivo models.

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Zhang, X., Satchell, M.A., Clark, R.S.B., Nathaniel, P.D., Kochanek, P.M., Graham, S.H. (2001). Apoptosis. In: Clark, R.S.B., Kochanek, P. (eds) Brain Injury. Molecular and Cellular Biology of Critical Care Medicine, vol 2. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1721-4_10

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