- Top of page
- APOPTOSIS IN PANCREATIC BETA-CELLS
- STIMULI OF APOPTOSIS IN PANCREATIC BETA-CELLS
- CASPASES: ACTIVATION AND PATHWAY
- FROM THE ACTIVATION OF CASPASES TO THE APOPTOTIC CHANGES IN THE MORPHOLOGY OF PANCREATIC BETA-CELLS
- STRATEGIES FOR PREVENTING APOPTOSIS OF ISLETS
- LITERATURE CITED
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.