炎症体在胰岛素抵抗和2型糖尿病发生中的作用。
Role of the inflammasome in insulin resistance and type 2 diabetes mellitus.
发表日期:2023
作者:
Shen Lu, Yanrong Li, Zhaojun Qian, Tiesuo Zhao, Zhiwei Feng, Xiaogang Weng, Lili Yu
来源:
Frontiers in Immunology
摘要:
炎性体是一种蛋白质复合体,由细胞中的多种蛋白质组成,参与体内的先天免疫反应。它可以通过上游信号调节激活,发挥重要作用于噬菌体、凋亡、炎症、肿瘤调节等方面。近年来,代谢综合征患者中胰岛素抵抗(IR)的人数逐年增多,炎性体与代谢性疾病的发生和发展密切相关。炎性体可以直接或间接影响胰岛素信号传导途径,参与IR和2型糖尿病(T2DM)的发生。此外,各种治疗剂也可以通过炎性体来治疗糖尿病。本综述重点介绍了炎性体在IR和T2DM中的作用,指出了它们之间的关联和实用价值。简言之,我们已经详细讨论了NLRP1、NLRP3、NLRC4、NLRP6和AIM2等主要炎性体,以及它们在IR中的结构、激活和调节方式。最后,我们讨论了目前与炎性体有关的治疗选择对于T2DM的治疗。特别地,与NLRP3相关的治疗剂和选项已经广泛开发。总之,本文回顾了炎性体在IR和T2DM中的作用和研究进展。版权所有 © 2023 Lu、Li、Qian、Zhao、Feng、Weng和Yu。
The inflammasome is a protein complex composed of a variety of proteins in cells and which participates in the innate immune response of the body. It can be activated by upstream signal regulation and plays an important role in pyroptosis, apoptosis, inflammation, tumor regulation, etc. In recent years, the number of metabolic syndrome patients with insulin resistance (IR) has increased year by year, and the inflammasome is closely related to the occurrence and development of metabolic diseases. The inflammasome can directly or indirectly affect conduction of the insulin signaling pathway, involvement the occurrence of IR and type 2 diabetes mellitus (T2DM). Moreover, various therapeutic agents also work through the inflammasome to treat with diabetes. This review focuses on the role of inflammasome on IR and T2DM, pointing out the association and utility value. Briefly, we have discussed the main inflammasomes, including NLRP1, NLRP3, NLRC4, NLRP6 and AIM2, as well as their structure, activation and regulation in IR were described in detail. Finally, we discussed the current therapeutic options-associated with inflammasome for the treatment of T2DM. Specially, the NLRP3-related therapeutic agents and options are widely developed. In summary, this article reviews the role of and research progress on the inflammasome in IR and T2DM.Copyright © 2023 Lu, Li, Qian, Zhao, Feng, Weng and Yu.