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系统性红斑狼疮中的cGAS-STING通路:生物学意义及治疗机遇

cGAS-STING pathway in systemic lupus erythematosus: biological implications and therapeutic opportunities.

作者信息

Feng Qun, Xu Xiaolin, Zhang Shoulin

机构信息

College of Chinese Medicine, Changchun University of Chinese Medicine, Changchun, 130017, China.

Cardiology Department, Affiliated Hospital of Changchun University of Chinese Medicine, Changchun, 130021, China.

出版信息

Immunol Res. 2024 Dec;72(6):1207-1216. doi: 10.1007/s12026-024-09525-1. Epub 2024 Aug 3.

DOI:10.1007/s12026-024-09525-1
PMID:39096420
Abstract

The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) signaling pathway has been identified as a significant modulator of inflammation in various clinical contexts, including infection, cellular stress, and tissue injury. The extensive participation of the cGAS-STING pathway can be attributed to its ability to detect and control the cellular reaction to DNAs originating from both microorganisms and hosts. These DNAs are well recognized as molecules linked with potential risks. At physiological levels, the STING signaling system exhibits protective effects. However, prolonged stimulation of this pathway contributes to autoimmune disorder pathogenesis. The present paper provides an overview of the activation mechanism of the cGAS-STING signaling pathways and their associated significant functions, as well as therapeutic interventions in the context of systemic lupus erythematosus (SLE). The primary objective is to enhance our comprehension of SLE and facilitate more effective diagnosis and treatment strategies for this condition.

摘要

环磷酸鸟苷-腺苷酸合成酶(cGAS)-干扰素基因刺激因子(STING)信号通路已被确定为多种临床情况下炎症的重要调节因子,包括感染、细胞应激和组织损伤。cGAS-STING通路的广泛参与可归因于其检测和控制细胞对源自微生物和宿主的DNA反应的能力。这些DNA被公认为与潜在风险相关的分子。在生理水平上,STING信号系统具有保护作用。然而,该通路的长期刺激会导致自身免疫性疾病的发病机制。本文概述了cGAS-STING信号通路的激活机制及其相关的重要功能,以及系统性红斑狼疮(SLE)背景下的治疗干预措施。主要目的是加深我们对SLE的理解,并促进针对这种疾病更有效的诊断和治疗策略。

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Mitochondrial Lon protease promotes CD4 T cell activation by activating the cGAS-STING-TBK1 axis in systemic lupus erythematosus.线粒体 Lon 蛋白酶通过激活系统性红斑狼疮中的 cGAS-STING-TBK1 轴促进 CD4 T 细胞活化。
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