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β ‐Cell inflammation in human type 2 diabetes and the role of autophagy
Author(s) -
Marselli L.,
Bugliani M.,
Suleiman M.,
Olimpico F.,
Masini M.,
Petrini M.,
Boggi U.,
Filipponi F.,
Syed F.,
Marchetti P.
Publication year - 2013
Publication title -
diabetes, obesity and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.445
H-Index - 128
eISSN - 1463-1326
pISSN - 1462-8902
DOI - 10.1111/dom.12152
Subject(s) - autophagy , inflammation , chemokine , immune system , islet , apoptosis , immunology , cell type , biology , microbiology and biotechnology , type 2 diabetes , diabetes mellitus , type 1 diabetes , cancer research , cell , endocrinology , genetics
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.