遗传 ›› 2022, Vol. 44 ›› Issue (10): 840-852.doi: 10.16288/j.yczz.22-265
收稿日期:
2022-08-04
修回日期:
2022-09-02
出版日期:
2022-10-20
发布日期:
2022-09-30
通讯作者:
孟卓贤
E-mail:3190100992@zju.edu.cn;zxmeng@zju.edu.cn
基金资助:
Chengan Lv1,2(), Ruoran Wang1,2, Zhuo-Xian Meng1,2()
Received:
2022-08-04
Revised:
2022-09-02
Online:
2022-10-20
Published:
2022-09-30
Contact:
Meng Zhuo-Xian
E-mail:3190100992@zju.edu.cn;zxmeng@zju.edu.cn
Supported by:
摘要:
近年来,2型糖尿病(type 2 diabetes,T2D)发病率迅速上升,已成为全球性的健康危机。最近的临床和基础研究表明,胰岛β细胞功能障碍是导致T2D及其相关并发症的重要原因。在2型糖尿病的自然病程中,胰岛β细胞经历从代偿到失代偿的动态变化;其中,代谢应激反应,如内质网应激(endoplasmic reticulum stress,ER stress)、氧化应激(oxidative stress)和炎症(inflammation)是β细胞功能变化的关键调控机制。本文总结了β细胞功能在2型糖尿病病程中动态变化的研究进展,以期深化对2型糖尿病分子机制的理解,为精准诊断和临床干预2型糖尿病提供参考。
吕承安, 王若然, 孟卓贤. 2型糖尿病进程中胰岛β细胞功能变化的分子机制[J]. 遗传, 2022, 44(10): 840-852.
Chengan Lv, Ruoran Wang, Zhuo-Xian Meng. Molecular mechanism of islet β-cell functional alternations during type 2 diabetes[J]. Hereditas(Beijing), 2022, 44(10): 840-852.
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