Title:Role of Pancreatic β-Cell Death and Cell Death-Associated Inflammation in Diabetes
Volume: 12
Issue: 10
Author(s): M.-S. Lee, K.-A. Kim and H.S. Kim
Affiliation:
Keywords:
Apoptosis, autophagy, β-cell death, diabetes, innate immunity, necrosis, autoimmune disorder, hypoinsulinemia, hyperglycemia, antigen-presenting cells, insulin deficiency, lipotoxicity, lipoapoptosis, pancreatic β-cells, inflammation
Abstract: Pancreatic β-cell death of various types has diverse and important roles in the pathogenesis of both
type 1 (T1D) and type 2 (T2D) diabetes. The most widely recognized types of β-cell death in diabetes are
apoptosis (type 1 programmed cell death) and necrosis. Apoptosis of β-cells is the key and final step in the
development of T1D and contributes to β-cell failure or dysfunction in T2D. In the course of natural T1D,
apoptotic β-cells undergoing secondary necrosis probably due to their defective clearance by phagocytes, may
be involved in the initiation and development of the disease. Recently, autophagy (type 2 programmed cell
death) is proposed as a third type of cell death and is being recognized as having certain roles in the
prevention and execution of β-cell death, depending on the cellular context. Moreover, as dying β-cells are
routinely exposed to the immune system, β-cell death could also affect the development of diabetes through
regulation of inflammation or immune response. In this review, we describe the role of various types of
pancreatic β-cell death in the development of T1D and T2D. We also discuss the role of dying β-cells in the
control of inflammation which contributes to the pathogenesis of diabetes.
