Long non-coding RNAs as key modulators of pancreatic β-cell mass and function

Numerous studies have sought to decipher the genetic and other mechanisms contributing to β-cell loss and dysfunction in diabetes mellitus. However, we have yet to fully understand the etiology of the disease or to develop satisfactory treatments. Since the majority of diabetes susceptibility loci a...

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Main Authors: López-Noriega, Livia, Rutter, Guy A.
Other Authors: Lee Kong Chian School of Medicine (LKCMedicine)
Format: Article
Language:English
Published: 2021
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Online Access:https://hdl.handle.net/10356/152054
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spelling sg-ntu-dr.10356-1520542023-03-05T16:43:52Z Long non-coding RNAs as key modulators of pancreatic β-cell mass and function López-Noriega, Livia Rutter, Guy A. Lee Kong Chian School of Medicine (LKCMedicine) Science::Medicine Long Non-Coding RNA Beta Cell Numerous studies have sought to decipher the genetic and other mechanisms contributing to β-cell loss and dysfunction in diabetes mellitus. However, we have yet to fully understand the etiology of the disease or to develop satisfactory treatments. Since the majority of diabetes susceptibility loci are mapped to non-coding regions within the genome, understanding the functions of non-coding RNAs in β-cell biology might provide crucial insights into the pathogenesis of type 1 (T1D) and type 2 (T2D) diabetes. During the past decade, numerous studies have indicated that long non-coding RNAs play important roles in the maintenance of β-cell mass and function. Indeed, lncRNAs have been shown to be involved in controlling β-cell proliferation during development and/or β-cell compensation in response to hyperglycaemia. LncRNAs such as TUG-1 and MEG3 play a role in both β-cell apoptosis and function, while others sensitize β-cells to apoptosis in response to stress signals. In addition, several long non-coding RNAs have been shown to regulate the expression of β-cell-enriched transcription factors in cis or in trans. In this review, we provide an overview of the roles of lncRNAs in maintaining β-function and mass, and discuss their relevance in the development of diabetes. Published version GAR was supported by a Wellcome Trust Investigator Award (212625/Z/18/Z), MRC Programme grants (MR/R022259/1, MR/J0003042/1, MR/L020149/1) and by Diabetes UK (BDA/11/0004210, BDA/15/0005275, BDA 16/0005485) project grants. This project has received funding from the European Union’s Horizon 2020 research and innovation programme via the Innovative Medicines Initiative 2 Joint Undertaking under grant agreement No 115881 (RHAPSODY). This Joint Undertaking receives support from the European Union’s Horizon 2020 research and innovation programme and EFPIA. 2021-11-18T06:19:38Z 2021-11-18T06:19:38Z 2021 Journal Article López-Noriega, L. & Rutter, G. A. (2021). Long non-coding RNAs as key modulators of pancreatic β-cell mass and function. Frontiers in Endocrinology, 11, 610213-. https://dx.doi.org/10.3389/fendo.2020.610213 1664-2392 https://hdl.handle.net/10356/152054 10.3389/fendo.2020.610213 33628198 2-s2.0-85101266301 11 610213 en Frontiers in Endocrinology © 2021 López–Noriega and Rutter. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. application/pdf
institution Nanyang Technological University
building NTU Library
continent Asia
country Singapore
Singapore
content_provider NTU Library
collection DR-NTU
language English
topic Science::Medicine
Long Non-Coding RNA
Beta Cell
spellingShingle Science::Medicine
Long Non-Coding RNA
Beta Cell
López-Noriega, Livia
Rutter, Guy A.
Long non-coding RNAs as key modulators of pancreatic β-cell mass and function
description Numerous studies have sought to decipher the genetic and other mechanisms contributing to β-cell loss and dysfunction in diabetes mellitus. However, we have yet to fully understand the etiology of the disease or to develop satisfactory treatments. Since the majority of diabetes susceptibility loci are mapped to non-coding regions within the genome, understanding the functions of non-coding RNAs in β-cell biology might provide crucial insights into the pathogenesis of type 1 (T1D) and type 2 (T2D) diabetes. During the past decade, numerous studies have indicated that long non-coding RNAs play important roles in the maintenance of β-cell mass and function. Indeed, lncRNAs have been shown to be involved in controlling β-cell proliferation during development and/or β-cell compensation in response to hyperglycaemia. LncRNAs such as TUG-1 and MEG3 play a role in both β-cell apoptosis and function, while others sensitize β-cells to apoptosis in response to stress signals. In addition, several long non-coding RNAs have been shown to regulate the expression of β-cell-enriched transcription factors in cis or in trans. In this review, we provide an overview of the roles of lncRNAs in maintaining β-function and mass, and discuss their relevance in the development of diabetes.
author2 Lee Kong Chian School of Medicine (LKCMedicine)
author_facet Lee Kong Chian School of Medicine (LKCMedicine)
López-Noriega, Livia
Rutter, Guy A.
format Article
author López-Noriega, Livia
Rutter, Guy A.
author_sort López-Noriega, Livia
title Long non-coding RNAs as key modulators of pancreatic β-cell mass and function
title_short Long non-coding RNAs as key modulators of pancreatic β-cell mass and function
title_full Long non-coding RNAs as key modulators of pancreatic β-cell mass and function
title_fullStr Long non-coding RNAs as key modulators of pancreatic β-cell mass and function
title_full_unstemmed Long non-coding RNAs as key modulators of pancreatic β-cell mass and function
title_sort long non-coding rnas as key modulators of pancreatic β-cell mass and function
publishDate 2021
url https://hdl.handle.net/10356/152054
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