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 β 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 β cell identity and suggest that miRNAs may function as important genetic components in metabolic disorders, including diabetes.
Keywords: cellular identity; dedifferentiation; diabetes; endocrine pancreas; miRNAs; β cells.
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