Full Text:
<293>
Summary: 
<106>
CLC number:
On-line Access: 2024-08-27
Received: 2023-10-17
Revision Accepted: 2024-05-08
Crosschecked: 2024-09-23
Cited: 0
Clicked: 553
Early senescence of pancreatic β cells induced by unfolded protein response deficiency prevents type 1 diabetes
| ||||||||||||||
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
ER -
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).
[1]EnginF, YermalovichA, NguyenT, et al., 2013. Restoration of the unfolded protein response in pancreatic β cells protects mice against type 1 diabetes. Sci Transl Med, 5(211):211ra156.
[2]Evans-MolinaC, SimsEK, DimeglioLA, et al., 2018. β Cell dysfunction exists more than 5 years before type 1 diabetes diagnosis. JCI Insight, 3(15):e120877.
[3]LeeH, LeeYS, HarendaQ, et al., 2020. Beta cell dedifferentiation induced by IRE1α deletion prevents type 1 diabetes. Cell Metab, 31(4):822-836.e5.
[4]LeeH, SahinGS, ChenCW, et al., 2023. Stress-induced β cell early senescence confers protection against type 1 diabetes. Cell Metab, 35(12):2200-2215.e9.
[5]LeendersF, GroenN, de GraafN, et al., 2021. Oxidative stress leads to β-cell dysfunction through loss of β-cell identity. Front Immunol, 12:690379.
[6]MakamAA, BiswasA, KothegalaL, et al., 2022. Setting the stage for insulin granule dysfunction during type-1-diabetes: is ER stress the culprit? Biomedicines, 10(11):2695.
[7]MoritaS, VillaltaSA, FeldmanHC, et al., 2017. Targeting ABL-IRE1α signaling spares ER-stressed pancreatic β cells to reverse autoimmune diabetes. Cell Metab, 25(4):883-897.e8.
[8]Paramos-de-CarvalhoD, JacintoA, SaúdeL, 2021. The right time for senescence. Elife, 10:e72449.
[9]ParsaR, AndresenP, GillettA, et al., 2012. Adoptive transfer of immunomodulatory M2 macrophages prevents type 1 diabetes in NOD mice. Diabetes, 61(11):2881-2892.
[10]RuiJX, DengSY, AraziA, et al., 2017. β Cells that resist immunological attack develop during progression of autoimmune diabetes in NOD mice. Cell Metab, 25(3):727-738.
[11]ShanB, WangXX, WuY, et al., 2017. The metabolic ER stress sensor IRE1α suppresses alternative activation of macrophages and impairs energy expenditure in obesity. Nat Immunol, 18(5):519-529.
[12]SturmlechnerI, ZhangC, SineCC, et al., 2021. P21 produces a bioactive secretome that places stressed cells under immunosurveillance. Science, 374(6567):eabb3420.
[13]SyedFZ, 2022. Type 1 diabetes mellitus. Ann Intern Med, 175(3):ITC33-ITC48.
[14]ThompsonPJ, ShahA, NtranosV, et al., 2019. Targeted elimination of senescent beta cells prevents type 1 diabetes. Cell Metab, 29(5):1045-1060.e10.
Open peer comments: Debate/Discuss/Question/Opinion
<1>