Role of caspases in the regulation of apoptotic pancreatic islet beta-cells death
Version of Record online: 13 FEB 2004
Copyright © 2004 Wiley-Liss, Inc.
Journal of Cellular Physiology
Volume 200, Issue 2, pages 177–200, August 2004
How to Cite
Hui, H., Dotta, F., Mario, U. D. and Perfetti, R. (2004), Role of caspases in the regulation of apoptotic pancreatic islet beta-cells death. J. Cell. Physiol., 200: 177–200. doi: 10.1002/jcp.20021
- Issue online: 27 MAY 2004
- Version of Record online: 13 FEB 2004
- Manuscript Accepted: 6 NOV 2003
- Manuscript Received: 1 OCT 2003
The homeostatic control of beta-cell mass in normal and pathological conditions is based on the balance of proliferation, differentiation, and death of the insulin-secreting cells. A considerable body of evidence, accumulated during the last decade, has emphasized the significance of the disregulation of the mechnanisms regulating the apoptosis of beta-cells in the sequence of events that lead to the development of diabetes. The identification of agents capable of interfering with this process needs to be based on a better understanding of the beta-cell specific pathways that are activated during apoptosis. The aim of this article is fivefold: (1) a review of the evidence for beta-cell apoptosis in Type I diabetes, Type II diabetes, and islet transplantation, (2) to review the common stimuli and their mechanisms in pancreatic beta-cell apoptosis, (3) to review the role of caspases and their activation pathway in beta-cell apoptosis, (4) to review the caspase cascade and morphological cellular changes in apoptotic beta-cells, and (5) to highlight the putative strategies for preventing pancreatic beta-cells from apoptosis. © 2004 Wiley-Liss, Inc.