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ER stress and development of type 1 diabetes

Feyza Engin
DOI: 10.1097/JIM.0000000000000229 Published 11 January 2016
Feyza Engin
Departments of Biomolecular Chemistry and Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI, USA
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Abstract

Type 1 diabetes (T1D) results from an autoimmune-mediated destruction of pancreatic β cells. The incidence of T1D is on the rise globally around 3% to 5% per year and rapidly increasing incidence in younger children is of the greatest concern. currently, there is no way to cure or prevent T1D; hence, a deeper understanding of the underlying molecular mechanisms of this disease is essential to the development of new effective therapies. The endoplasmic reticulum (ER) is an organelle with multiple functions that are essential for cellular homeostasis. Excessive demand on the ER, chronic inflammation, and environmental factors lead to ER stress and to re-establish cellular homeostasis, the adaptive unfolded protein response (UPR) is triggered. However, chronic ER stress leads to a switch from a prosurvival to a proapoptotic UPR, resulting in cell death. Accumulating data have implicated ER stress and defective UPR in the pathogenesis of inflammatory and autoimmune diseases, and ER stress has been implicated in β-cell failure in type 2 diabetes. However, the role of ER stress and the UPR in β-cell pathophysiology and in the initiation and propagation of the autoimmune responses in T1D remains undefined. This review will highlight the current understanding and recent in vivo data on the role of ER stress and adaptive responses in T1D pathogenesis and the potential therapeutic aspect of enhancing β-cell ER function and restoring UPR defects as novel clinical strategies against this disease.

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Vol 64 Issue 1 Table of Contents
Journal of Investigative Medicine: 64 (1)
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ER stress and development of type 1 diabetes
Feyza Engin
Journal of Investigative Medicine Jan 2016, 64 (1) 2-6; DOI: 10.1097/JIM.0000000000000229

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ER stress and development of type 1 diabetes
Feyza Engin
Journal of Investigative Medicine Jan 2016, 64 (1) 2-6; DOI: 10.1097/JIM.0000000000000229
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ER stress and development of type 1 diabetes
Feyza Engin
Journal of Investigative Medicine Jan 2016, 64 (1) 2-6; DOI: 10.1097/JIM.0000000000000229
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  • Article
    • Abstract
    • ENDOPLASMIC RETICULUM STRESS AND THE UNFOLDED PROTEIN RESPONSE
    • INFLAMMATION, AUTOIMMUNITY, AND THE UPR
    • ABERRANT UPR AND T1D
    • FUTURE DIRECTIONS
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