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. © 2013 John Wiley & Sons Ltd.
|Autori interni:||MARSELLI, LORELLA|
|Autori:||L. Marselli;M. Bugliani;M. Suleiman;F. Olimpico;M. Masini;M. Petrini;U. Boggi;F. Filipponi;F. Syed;P. Marchetti|
|Titolo:||β-Cell inflammation in human type 2 diabetes and the role of autophagy|
|Anno del prodotto:||2013|
|Digital Object Identifier (DOI):||10.1111/dom.12152|
|Appare nelle tipologie:||1.1 Articolo in rivista|