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High-Throughput Approaches Onto Uncover (Epi)Genomic Architecture of Type 2 Diabetes

Overview
Journal Genes (Basel)
Publisher MDPI
Date 2018 Jul 28
PMID 30050001
Citations 10
Authors
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Abstract

Type 2 diabetes (T2D) is a complex disorder that is caused by a combination of genetic, epigenetic, and environmental factors. High-throughput approaches have opened a new avenue toward a better understanding of the molecular bases of T2D. A genome-wide association studies (GWASs) identified a group of the most common susceptibility genes for T2D (i.e., , , , , , and ) and illuminated novel disease-causing pathways. Next-generation sequencing (NGS)-based techniques have shed light on rare-coding genetic variants that account for an appreciable fraction of T2D heritability ( and ) and population risk of T2D (, , , and ). Moreover, single-cell sequencing of human pancreatic islets identified gene signatures that are exclusive to α-cells (, , and ) and β-cells (, , , and ). Ongoing epigenome-wide association studies (EWASs) have progressively defined links between epigenetic markers and the transcriptional activity of T2D target genes. Differentially methylated regions were found in , , , , , , and loci that are related to T2D. Additionally, chromatin state maps in pancreatic islets were provided and several non-coding RNAs (ncRNA) that are key to T2D pathogenesis were identified (i.e., miR-375). The present review summarizes major progress that has been made in mapping the (epi)genomic landscape of T2D within the last few years.

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