Abstract
Type 2 diabetes (T2D) is caused by an inherited predisposition to pancreatic islet β-cell failure, which is manifested under cellular stress induced by metabolic overload. The decrease in the functional β-cell mass associated with T2D has been attributed primarily to β-cell death; however, studies in recent years suggested that β-cell dedifferentiation may contribute to this decline. The mechanisms linking genetic factors and cellular stress to β-cell dedifferentiation remain largely unknown. This study evaluated the evidence for β-cell dedifferentiation in T2D, and T2D and examined experimental systems in which its mechanisms may be studied. Understanding these mechanisms may allow prevention of β-cell dedifferentiation or induction of cell redifferentiation for restoration of the functional β-cell mass. Stem Cells 2019;37:1267-1272.
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