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Review

Endoplasmic Reticulum (ER) Stress and Its Role in Pancreatic β-Cell Dysfunction and Senescence in Type 2 Diabetes

by 1,2 and 1,2,3,*
1
Department of New Biology, Daegu Gyeongbuk Institute of Science and Technology (DGIST), Daegu 42988, Korea
2
New Biology Research Center, Daegu Gyeongbuk Institute of Science and Technology (DGIST), Daegu 42988, Korea
3
Well Aging Research Center, Daegu Gyeongbuk Institute of Science and Technology (DGIST), Daegu 42988, Korea
*
Author to whom correspondence should be addressed.
Academic Editor: Chunjung Chen
Int. J. Mol. Sci. 2022, 23(9), 4843; https://doi.org/10.3390/ijms23094843
Received: 5 April 2022 / Revised: 22 April 2022 / Accepted: 26 April 2022 / Published: 27 April 2022
(This article belongs to the Special Issue Endoplasmic Reticulum Stress-Related Biomedical Implications)
An increased life span and accompanying nutritional affluency have led to a rapid increase in diseases associated with aging, such as obesity and type 2 diabetes, imposing a tremendous economic and health burden on society. Pancreatic β-cells are crucial for controlling glucose homeostasis by properly producing and secreting the glucose-lowering hormone insulin, and the dysfunction of β-cells determines the outcomes for both type 1 and type 2 diabetes. As the native structure of insulin is formed within the endoplasmic reticulum (ER), ER homeostasis should be appropriately maintained to allow for the proper metabolic homeostasis and functioning of β-cells. Recent studies have found that cellular senescence is critically linked with cellular stresses, including ER stress, oxidative stress, and mitochondrial stress. These studies implied that β-cell senescence is caused by ER stress and other cellular stresses and contributes to β-cells’ dysfunction and the impairment of glucose homeostasis. This review documents and discusses the current understanding of cellular senescence, β-cell function, ER stress, its associated signaling mechanism (unfolded protein response), and the effect of ER stress on β-cell senescence and dysfunction. View Full-Text
Keywords: endoplasmic reticulum; ER stress; pancreatic beta cell; cellular senescence; type 2 diabetes; insulin; islet amyloid polypeptide endoplasmic reticulum; ER stress; pancreatic beta cell; cellular senescence; type 2 diabetes; insulin; islet amyloid polypeptide
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MDPI and ACS Style

Lee, J.-H.; Lee, J. Endoplasmic Reticulum (ER) Stress and Its Role in Pancreatic β-Cell Dysfunction and Senescence in Type 2 Diabetes. Int. J. Mol. Sci. 2022, 23, 4843. https://doi.org/10.3390/ijms23094843

AMA Style

Lee J-H, Lee J. Endoplasmic Reticulum (ER) Stress and Its Role in Pancreatic β-Cell Dysfunction and Senescence in Type 2 Diabetes. International Journal of Molecular Sciences. 2022; 23(9):4843. https://doi.org/10.3390/ijms23094843

Chicago/Turabian Style

Lee, Ji-Hye, and Jaemin Lee. 2022. "Endoplasmic Reticulum (ER) Stress and Its Role in Pancreatic β-Cell Dysfunction and Senescence in Type 2 Diabetes" International Journal of Molecular Sciences 23, no. 9: 4843. https://doi.org/10.3390/ijms23094843

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