Kaspi_2014_Trends.Endocrinol.Metab_25_285

Normal physiology depends on defined functional output of differentiated cells. However, differentiated cells are often surprisingly fragile. As an example, phenotypic collapse and dedifferentiation of beta cells were recently discovered in the pathogenesis of type 2 diabetes (T2D). These discoveries necessitate the investigation of mechanisms that function to maintain robust cell type identity. microRNAs (miRNAs), which are small non-coding RNAs, are known to impart robustness to development. miRNAs are interlaced within networks, that include also transcriptional and epigenetic regulators, for continuous control of lineage-specific gene expression. In this Opinion article, we provide a framework for conceptualizing how miRNAs might participate in adult beta cell identity and suggest that miRNAs may function as important genetic components in metabolic disorders, including diabetes.