Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2017 Jun;14(6):488-496.
doi: 10.1038/cmi.2017.7. Epub 2017 Mar 20.

miRNAs: novel regulators of autoimmunity-mediated pancreatic β-cell destruction in type 1 diabetes

Affiliations
Review

miRNAs: novel regulators of autoimmunity-mediated pancreatic β-cell destruction in type 1 diabetes

Ying Zheng et al. Cell Mol Immunol. 2017 Jun.

Abstract

MicroRNAs (miRNAs) are a series of conserved, short, non-coding RNAs that modulate gene expression in a posttranscriptional manner. miRNAs are involved in almost every physiological and pathological process. Type 1 diabetes (T1D) is an autoimmune disease that is the result of selective destruction of pancreatic β-cells driven by the immune system. miRNAs are also important participants in T1D pathogenesis. Herein, we review the most recent data on the potential involvement of miRNAs in T1D. Specifically, we focus on two aspects: the roles of miRNAs in maintaining immune homeostasis and regulating β-cell survival and/or functions in T1D. We also discuss circulating miRNAs as potent biomarkers for the diagnosis and prediction of T1D and investigate potential therapeutic approaches for this disease.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
miRNAs: new regulators of autoimmunity and pancreatic β-cell destruction in type 1 diabetes. miRNAs may regulate naïve T cell, Th cell (including Th1, Th2, Th17 and Treg cells), B cell and APC differentiation, proliferation, cell death and functions, consequently inducing the appearance of autoimmunity and causing β-cell destruction. These effects lead to the onset and development of type 1 diabetes. In addition, miRNA dysregulation may affect β-cell survival, functions and regeneration, thereby contributing to the pathogenesis of type 1 diabetes

References

    1. Anaya JM. The diagnosis and clinical significance of polyautoimmunity. Autoimmun Rev 2014; 13: 423–426. - PubMed
    1. Kahaly GJ, Hansen MP. Type 1 diabetes associated autoimmunity. Autoimmun Rev 2016; 15: 644–648. - PubMed
    1. Morran MP, Omenn GS, Pietropaolo M. Immunology and genetics of type 1 diabetes. Mt Sinai J Med 2008; 75: 314–327. - PubMed
    1. Stankov K, Benc D, Draskovic D. Genetic and epigenetic factors in etiology of diabetes mellitus type 1. Pediatrics 2013; 132: 1112–1122. - PubMed
    1. Simmons KM, Gottlieb PA, Michels AW. Immune intervention and preservation of pancreatic beta cell function in type 1 diabetes. Curr Diab Rep 2016; 16: 97. - PMC - PubMed