PMID- 34630329
OWN - NLM
STAT- MEDLINE
DCOM- 20220211
LR  - 20240403
IS  - 1664-2392 (Print)
IS  - 1664-2392 (Electronic)
IS  - 1664-2392 (Linking)
VI  - 12
DP  - 2021
TI  - Epigenetic Regulation of beta Cell Identity and Dysfunction.
PG  - 725131
LID - 10.3389/fendo.2021.725131 [doi]
LID - 725131
AB  - beta cell dysfunction and failure are driving forces of type 2 diabetes mellitus 
      (T2DM) pathogenesis. Investigating the underlying mechanisms of beta 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 beta cell identity during embryonic development, postnatal maturation, and 
      maintain beta cell function at homeostatic states. During progression of T2DM, 
      overnutrition, inflammation, and other types of stress collaboratively disrupt 
      the homeostatic epigenetic signatures in beta cells. Dysregulated epigenetic 
      signatures, and the associating transcriptional outputs, lead to the dysfunction 
      and eventual loss of beta cells. In this review, we will summarize recent 
      discoveries of the establishment and disruption of beta cell-specific epigenetic 
      signatures, and discuss the potential implication in therapeutic development.
CI  - Copyright (c) 2021 Sun, Wang, Obayomi and Wei.
FAU - Sun, Xiaoqiang
AU  - Sun X
AD  - Department of Physiology and Biomedical Engineering, Mayo Clinic Arizona, 
      Scottsdale, AZ, United States.
AD  - Tianjin Fourth Central Hospital, Tianjin, China.
AD  - The Fourth Central Hospital Affiliated to Nankai University, Tianjin, China.
AD  - The Fourth Central Hospital Clinical College, Tianjin Medical University, 
      Tianjin, China.
FAU - Wang, Liu
AU  - Wang L
AD  - Department of Physiology and Biomedical Engineering, Mayo Clinic Arizona, 
      Scottsdale, AZ, United States.
FAU - Obayomi, S M Bukola
AU  - Obayomi SMB
AD  - Department of Physiology and Biomedical Engineering, Mayo Clinic Arizona, 
      Scottsdale, AZ, United States.
FAU - Wei, Zong
AU  - Wei Z
AD  - Department of Physiology and Biomedical Engineering, Mayo Clinic Arizona, 
      Scottsdale, AZ, United States.
LA  - eng
GR  - K01 DK120808/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20210924
PL  - Switzerland
TA  - Front Endocrinol (Lausanne)
JT  - Frontiers in endocrinology
JID - 101555782
RN  - 0 (Chromatin)
RN  - 0 (Histones)
SB  - IM
MH  - Animals
MH  - Chromatin/*genetics/metabolism
MH  - *DNA Methylation
MH  - Diabetes Mellitus, Type 1/genetics/metabolism/*pathology
MH  - Diabetes Mellitus, Type 2/genetics/metabolism/*pathology
MH  - *Epigenesis, Genetic
MH  - *Gene Expression Regulation
MH  - Histones/genetics/metabolism
MH  - Humans
MH  - Insulin-Secreting Cells/metabolism/*pathology
PMC - PMC8498190
OTO - NOTNLM
OT  - DNA methylation
OT  - beta cell dysfunction
OT  - chromatin accessibility
OT  - epigenetic
OT  - histone acetylation
OT  - non-coding RNAs
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2021/10/12 06:00
MHDA- 2022/02/12 06:00
PMCR- 2021/01/01
CRDT- 2021/10/11 05:55
PHST- 2021/06/14 00:00 [received]
PHST- 2021/09/08 00:00 [accepted]
PHST- 2021/10/11 05:55 [entrez]
PHST- 2021/10/12 06:00 [pubmed]
PHST- 2022/02/12 06:00 [medline]
PHST- 2021/01/01 00:00 [pmc-release]
AID - 10.3389/fendo.2021.725131 [doi]
PST - epublish
SO  - Front Endocrinol (Lausanne). 2021 Sep 24;12:725131. doi: 
      10.3389/fendo.2021.725131. eCollection 2021.