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Caspases and Their Natural Inhibitors as Therapeutic Targets for Regulating Apoptosis

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Book cover Proteases as Targets for Therapy

Part of the book series: Handbook of Experimental Pharmacology ((HEP,volume 140))

Abstract

Apoptosis, or programmed cell death, is a physiological cell suicide program that occurs in all animal species (STELLER 1995). Apoptosis ensures that the genesis of new cells via division is appropriately controlled and offset by cell loss. Cell death is a natural accompaniment of the physiology of fully differentiated cells in the skin, intestine, immune system, mammary gland and uterus. Developmental organization requires removal of many cells for achieving the final desired structures and ensures proper cyto-architectures of most organs such as the kidney, heart and brain. Moreover, elimination of cells that have been compromised by viral infection, oxidation, hypoxia and DNA damage is important for maintaining healthy tissues. Thus, it can be appreciated that dysfunctional programmed cell death contributes to several human diseases (DUKE et al. 1998). An illustration of this concept is that apoptotic defects appear to be the primary lesion in some types of cancer and leukemia, allowing malignant cells to survive longer than their intended life span and endowing these cells with a selective survival advantage relative to their normal counterparts. Therefore, cell death can contribute to neoplastic expansion in the absence of increased cellular division (REED 1998). Multiple examples exist where excessive apoptosis has been implicated with human disease including acquired immunodeficiency syndrome (AIDS), Alzheimer’s disease, myocardial infarction and stroke (DUKE et al. 1998).

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© 2000 Springer-Verlag Berlin Heidelberg

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Deveraux, Q.L., Reed, J.C., Salvesen, G.S. (2000). Caspases and Their Natural Inhibitors as Therapeutic Targets for Regulating Apoptosis. In: von der Helm, K., Korant, B.D., Cheronis, J.C. (eds) Proteases as Targets for Therapy. Handbook of Experimental Pharmacology, vol 140. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-57092-6_17

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  • DOI: https://doi.org/10.1007/978-3-642-57092-6_17

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