Role of caspases in the regulation of apoptotic pancreatic islet beta-cells death

J Cell Physiol. 2004 Aug;200(2):177-200. doi: 10.1002/jcp.20021.


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 mechanisms 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.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis*
  • Caspases / metabolism*
  • Diabetes Mellitus / pathology
  • Diabetes Mellitus / physiopathology*
  • Enzyme Activation
  • Humans
  • Islets of Langerhans / cytology
  • Islets of Langerhans / metabolism*
  • Models, Biological
  • Pancreas / cytology*


  • Caspases