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细胞焦亡在自身免疫性疾病发病机制中的作用。

The roles of pyroptosis in the pathogenesis of autoimmune diseases.

作者信息

Song Yingqiu, Peng Yanhui, Wang Bing, Zhou Xinyue, Cai Yikang, Chen Haiyong, Miao Chenggui

机构信息

Center for Xin'an Medicine and Modernization of Traditional Chinese Medicine of IHM, Anhui University of Chinese Medicine, Hefei, Anhui, China; Department of Pharmacology, School of Integrated Chinese and Western Medicine, Anhui University of Chinese Medicine, Hefei, Anhui, China.

School of Chinese Medicine, Li Ka Shing Faculty of Medicine, the University of Hong Kong, Hong Kong.

出版信息

Life Sci. 2024 Dec 15;359:123232. doi: 10.1016/j.lfs.2024.123232. Epub 2024 Nov 12.

Abstract

The occurrence of autoimmune diseases is a result of the immune system's immune response against healthy components of the body. Pyroptosis is an innovative form of programmed cell death dependent on inflammatory caspases, leading to the release of cytokines. Excessive pyroptosis can lead to a sustained inflammatory response, which may aggravate the development of autoimmune diseases. In rheumatoid arthritis (RA), tumor necrosis factor (TNF) and NLRP3 enhance pyroptosis, exacerbating the disease. In systemic lupus erythematosus (SLE), the release of nuclear antigen promotes the development of SLE. In multiple sclerosis (MS), elevated active caspase-11 in primary astrocytes induces oligodendrocyte pyroptosis, advancing MS progression. This review outlines the mechanisms of pyroptosis in autoimmune diseases. Meanwhile, we elaborated the possible therapeutic targets from the perspective of pyroptosis. We conclude that pyroptosis is expected to be a therapeutic target for autoimmune diseases.

摘要

自身免疫性疾病的发生是免疫系统针对身体健康成分产生免疫反应的结果。细胞焦亡是一种依赖于炎性半胱天冬酶的程序性细胞死亡的创新形式,会导致细胞因子的释放。过度的细胞焦亡会导致持续的炎症反应,这可能会加重自身免疫性疾病的发展。在类风湿性关节炎(RA)中,肿瘤坏死因子(TNF)和NLRP3会增强细胞焦亡,使病情恶化。在系统性红斑狼疮(SLE)中,核抗原的释放会促进SLE的发展。在多发性硬化症(MS)中,原代星形胶质细胞中活性半胱天冬酶-11的升高会诱导少突胶质细胞焦亡,推动MS的进展。本综述概述了自身免疫性疾病中细胞焦亡的机制。同时,我们从细胞焦亡的角度阐述了可能的治疗靶点。我们得出结论,细胞焦亡有望成为自身免疫性疾病的治疗靶点。

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