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

doi:10.1631/jzus.B2400013

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Correspondence | Updated：2024-09-20

Early senescence of pancreatic β cells induced by unfolded protein response deficiency prevents type 1 diabetes
Early senescence of pancreatic β cells induced by unfolded protein response deficiency prevents type 1 diabetes
未折叠蛋白应答缺失导致的胰岛β细胞早期衰老可预防1型糖尿病
Journal of Zhejiang University-SCIENCE B (Biomedicine & Biotechnology) Vol. 25, Issue 9, Pages: 796-799(2024)
Affiliations：

1.Department of Pathology, the Second Xiangya Hospital, Central South University, Changsha 410011, China
2.Institute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, Hunan International Scientific and Technological Cooperation Base of Arteriosclerotic Disease, Department of Bioinformatics and Medical Big Data, Hengyang Medical School, University of South China, Hengyang 421001, China
3.School of Basic Medicine, Health Science Center, Hubei University of Arts and Science, Xiangyang 441053, China
4.Guangxi Key Laboratory of Diabetic Systems Medicine, Guilin Medical University, Guilin 541199, China
5.Medical Education Department, Guangdong Provincial People’s Hospital, Zhuhai Hospital (Jinwan Central Hospital of Zhuhai), Zhuhai 519041, China
Funds：
DOI：10.1631/jzus.B2400013
CLC：
CSTR：
Published： 15 September 2024 ，

Received： 12 January 2024 ，
Accepted：

成海鹏,赵真旺,刘丹等.未折叠蛋白应答缺失导致的胰岛β细胞早期衰老可预防1型糖尿病[J].浙江大学学报（英文版）（B辑：生物医学和生物技术）,2024,25(09):796-799.

Haipeng CHENG, Zhenwang ZHAO, Dan LIU, et al. Early senescence of pancreatic β cells induced by unfolded protein response deficiency prevents type 1 diabetes. [J]. Journal of Zhejiang University-SCIENCE B (Biomedicine & Biotechnology) 25(9):796-799(2024)
成海鹏,赵真旺,刘丹等.未折叠蛋白应答缺失导致的胰岛β细胞早期衰老可预防1型糖尿病[J].浙江大学学报（英文版）（B辑：生物医学和生物技术）,2024,25(09):796-799. DOI： 10.1631/jzus.B2400013.

Haipeng CHENG, Zhenwang ZHAO, Dan LIU, et al. Early senescence of pancreatic β cells induced by unfolded protein response deficiency prevents type 1 diabetes. [J]. Journal of Zhejiang University-SCIENCE B (Biomedicine & Biotechnology) 25(9):796-799(2024) DOI： 10.1631/jzus.B2400013.

摘要

1型糖尿病（T1D）是T细胞介导的自身免疫性疾病，可导致胰腺β细胞的破坏和胰岛素分泌的不足。内质网（ER）是负责蛋白质合成、加工和分泌的重要细胞器。蛋白质合成的大量需求与蛋白质折叠能力之间的不平衡会导致ER应激，并过度激活未折叠蛋白应答（UPR）的三条经典通路：肌醇需求酶1α（IRE1α）、激活转录因子6（ATF6）和蛋白激酶RNA样内质网激酶（PERK）。为了探究UPR在T1D中的作用，有研究表明在非肥胖型糖尿病（NOD）小鼠的β细胞中特异性敲除ATF6和IRE1α会引起β细胞早期衰老，进一步改变β细胞的衰老相关分泌表型，继而募集M2型巨噬细胞至胰岛。最终，M2型巨噬细胞将促进免疫监视并清除终末衰老的β细胞，从而保护β细胞功能并降低T1D发病率。

Abstract

关键词

未折叠蛋白应答（UPR）衰老1型糖尿病（T1D）

Keywords

references

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