Endoplasmic Reticulum (ER) Stress and Its Role in Pancreatic β-Cell Dysfunction and Senescence in Type 2 Diabetes
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
▼
Show Figures
Figure 1
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited
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 StyleLee, 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
Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.
