β-Cell failure is crucial for the onset and progression of human type 2 diabetes, and a few studies have suggested that inflammation may play a role. Immune cell infiltration has been reported in subpopulations of islets in some cases of human type 2 diabetes, and altered gene expression of a few cytokines and chemokines has been observed in isolated islets and laser captured β-cells from diabetic subjects. Recent observations on the links between inflammation, apoptosis and autophagy are putting the focus on the possibility that modulating the autophagic processes could protect the β-cells from cytotoxicity induced by inflammatory mediators.
Keywords: autophagy; inflammation; pancreatic islets; type 2 diabetes; β-cells.
© 2013 John Wiley & Sons Ltd.