Epigenetic Regulation of β Cell Identity and Dysfunction

Xiaoqiang Sun, Liu Wang, S. M.Bukola Obayomi, Zong Wei

Research output: Contribution to journalReview articlepeer-review

Abstract

β cell dysfunction and failure are driving forces of type 2 diabetes mellitus (T2DM) pathogenesis. Investigating the underlying mechanisms of β cell dysfunction may provide novel targets for the development of next generation therapy for T2DM. Epigenetics is the study of gene expression changes that do not involve DNA sequence changes, including DNA methylation, histone modification, and non-coding RNAs. Specific epigenetic signatures at all levels, including DNA methylation, chromatin accessibility, histone modification, and non-coding RNA, define β cell identity during embryonic development, postnatal maturation, and maintain β cell function at homeostatic states. During progression of T2DM, overnutrition, inflammation, and other types of stress collaboratively disrupt the homeostatic epigenetic signatures in β cells. Dysregulated epigenetic signatures, and the associating transcriptional outputs, lead to the dysfunction and eventual loss of β cells. In this review, we will summarize recent discoveries of the establishment and disruption of β cell-specific epigenetic signatures, and discuss the potential implication in therapeutic development.

Original languageEnglish (US)
Article number725131
JournalFrontiers in Endocrinology
Volume12
DOIs
StatePublished - Sep 24 2021

Keywords

  • beta cell dysfunction
  • chromatin accessibility
  • DNA methylation
  • epigenetic
  • histone acetylation
  • non-coding RNAs

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism

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