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On-line Access: 2024-08-27
Received: 2023-10-17
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Early senescence of pancreatic β cells induced by unfolded protein response deficiency prevents type 1 diabetes
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Haipeng CHENG, Zhenwang ZHAO, Dan LIU, Yufei WANG, Min ZHANG. Early senescence of pancreatic β cells induced by unfolded protein response deficiency prevents type 1 diabetes[J]. Journal of Zhejiang University Science B, 2024, 25(9): 796-799.
@article{title="Early senescence of pancreatic β cells induced by unfolded protein response deficiency prevents type 1 diabetes",
author="Haipeng CHENG, Zhenwang ZHAO, Dan LIU, Yufei WANG, Min ZHANG",
journal="Journal of Zhejiang University Science B",
volume="25",
number="9",
pages="796-799",
year="2024",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B2400013"
}
%0 Journal Article
%T Early senescence of pancreatic β cells induced by unfolded protein response deficiency prevents type 1 diabetes
%A Haipeng CHENG
%A Zhenwang ZHAO
%A Dan LIU
%A Yufei WANG
%A Min ZHANG
%J Journal of Zhejiang University SCIENCE B
%V 25
%N 9
%P 796-799
%@ 1673-1581
%D 2024
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B2400013
TY - JOUR
T1 - Early senescence of pancreatic β cells induced by unfolded protein response deficiency prevents type 1 diabetes
A1 - Haipeng CHENG
A1 - Zhenwang ZHAO
A1 - Dan LIU
A1 - Yufei WANG
A1 - Min ZHANG
J0 - Journal of Zhejiang University Science B
VL - 25
IS - 9
SP - 796
EP - 799
%@ 1673-1581
Y1 - 2024
PB - Zhejiang University Press & Springer
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DOI - 10.1631/jzus.B2400013
Abstract: type 1 diabetes (T1D) is a T lymphocyte-mediated autoimmune disease caused by pancreatic β-cell destruction, which eventually leads to reduced insulin level and increased blood glucose level (Syed, 2022). As a multifactorial disease, T1D is characterized by a genetic predisposition associated with various environmental and cellular elements (Syed, 2022). Pancreatic β cells have long been considered the “innocent victims” in T1D pathogenesis since the pancreas is attacked by the immune cells, resulting in a process known as insulitis, in which the immune cells infiltrate pancreatic islets and secrete pro-inflammatory cytokines. However, growing evidence suggests that various β-cell stresses, dysfunction, and death contribute to T1D pathogenesis, as it has been observed that β-cell dysfunction in autoantibody-positive (Aab+) individuals exists long before T1D diagnosis (Evans-Molina et al., 2018).
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