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6 - The regulation of vascular smooth muscle cell apoptosis
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- By Nicola J. McCarthy, Martin R. Bennett, Unit of Cardiovascular Medicine, Addenbrooke's Hospital, Cambridge
- Edited by Beverley J. Hunt, University of London, Lucilla Poston, University of London, Michael Schachter, Imperial College of Science, Technology and Medicine, London, Alison W. Halliday, St George's Hospital, London
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- Book:
- An Introduction to Vascular Biology
- Published online:
- 07 September 2009
- Print publication:
- 25 July 2002, pp 114-128
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- Chapter
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Summary
Introduction
Apoptosis or programmed cell death is a process through which multicellular organisms dispose of cells efficiently. Much has been discovered about the molecular control of apoptosis since its initial description as a series of morphological events (Kerr et al., 1972). The regulation of cell death is critical for the maintenance of tissue homeostasis. Moreover, it is apparent that all cells are programmed to die, and cell death is their default state, which can be suppressed through the expression or presence of intracellular and extracellular survival factors. Although it may seem strange that cells can be lost so easily from tissues, for long-lived multicellular organisms it makes biological sense to have an efficient cellular disposal mechanism, to remove useless or potentially harmful cells.
Apoptosis: defining the mode of cell death
Apoptosis defines a type of cell death distinct from conventional necrotic death, on the basis of characteristic morphological features (Figure 6.1). Specifically, these features are condensation of nuclear chromatin, at first around the inner face of the nuclear membrane, and then clumping of the chromatin. Apoptosis is also associated with loss of cell–cell contact and cell shrinkage and fragmentation, with formation of membrane-bound processes and vesicles containing fragments of nuclear material or organelles. The endproduct, the apoptotic body, may then be phagocytosed by adjacent cells (Figure 6.1). The whole process occurs with minimal disruption of membrane integrity or release of lysosomal enzymes, and consequently little inflammatory reaction.