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4 - Role of apoptosis in the pathophysiology of aplastic anemia

from Part I - Pathophysiology of acquired aplastic anemia

Published online by Cambridge University Press:  18 August 2009

E. C. Gordon-Smith
Affiliation:
St George's Hospital Medical School, London
Hubert Schrezenmeier
Affiliation:
Freie Universität Berlin
Andrea Bacigalupo
Affiliation:
Ospedale San Martino, Genoa
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Summary

Introduction

Apoptosis is the term coined for the morphologically distinct form of cell death that occurs under primarily physiological conditions (Kerr et al., 1972). Dysregulation of apoptosis (increased or decreased) is believed to be involved in the pathogenesis of a number of diverse disease states, including malignancy (Vaux, 1993; Williams, 1991), acquired immunodeficiency syndrome (AIDS) (Amieson, 1992; Amiesen and Capron, 1991; Martin, 1993) and neurodegenerative disorders, such as Alzheimer's disease and Parkinson's disease (Carson and Ribeiro, 1993; Loo et al., 1993). In multicellular organisms, the rate of cell death must be as tightly controlled as the rate of proliferation and differentiation. Apoptosis is the morphological term to describe cell death as a consequence of a signal from within the cell itself, and is important in embryogenesis (Lockshin et al., 1991), in aging (Newman et al., 1982) and for eliminating cells that are potentially harmful to the whole organism; for example, virally infected, autoreactive or damaged cells (Martin and Green, 1995). In mammalian systems, apoptosis is also readily observed after a number of pathological insults such as cytotoxic drugs or irradiation.

Apoptosis is a critical process in the regulation of cellular proliferation and differentiation. The majority of cells depend on the presence of specific survival factors to inhibit apoptosis; competition for these survival factors ensures a balance between cell division and cell death within a tissue, organ or organism.

Type
Chapter
Information
Aplastic Anemia
Pathophysiology and Treatment
, pp. 58 - 74
Publisher: Cambridge University Press
Print publication year: 1999

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