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Metabolic reprogramming as a key regulator in the pathogenesis of rheumatoid arthritis.
Inflammation Research ( IF 6.7 ) Pub Date : 2020-08-14 , DOI: 10.1007/s00011-020-01391-5
Wei-Wei Cai 1 , Yun Yu 1 , Shi-Ye Zong 1 , Fang Wei 1
Affiliation  

Purpose

Rheumatoid arthritis (RA) is a chronic, systemic autoimmune disease with synovitis as pathological changes. The immune microenvironment of RA promotes metabolic reprogramming of immune cells and stromal cells, which leads to dysfunction and imbalance of immune homeostasis. Cell metabolism undergoes the switch from a static regulatory state to a highly metabolic active state, which changes the redox-sensitive signaling pathway and also leads to the accumulation of metabolic intermediates, which in turn can act as signaling molecules and further aggravate the inflammatory response. The reprogramming of immunometabolism affects the function of immune cells and is crucial to the pathogenesis of RA. In addition, mitochondrial dysfunction plays a key role in glycolytic reprogramming in RA. These metabolic changes may be potential therapeutic targets for RA. Therefore, we reviewed the metabolic reprogramming of RA immune cells and fibroblast-like synovium cells (FLS) and its relationship with mitochondrial dysfunction.

Methods

A computer-based online search was performed using the PubMed database and Web of Science database for published articles concerning immunometabolic reprogramming, mitochondrial dysfunction, and rheumatoid arthritis.

Results

This article reviews the metabolic reprogramming of immune cells and fibroblast-like synoviocytes in RA and their relationship to mitochondrial disfunction, as well as the key pro-inflammatory pathways associated with metabolic reprogramming and chemotherapy as a potential future therapeutic strategy for RA.



中文翻译:

代谢重编程作为类风湿性关节炎发病机制的关键调节剂。

目的

类风湿性关节炎(RA)是一种以滑膜炎为病理改变的慢性全身性自身免疫性疾病。RA的免疫微环境促进免疫细胞和基质细胞的代谢重编程,导致免疫稳态失调和功能失调。细胞代谢从静态调控状态转变为高度代谢活跃状态,改变氧化还原敏感的信号通路,也导致代谢中间体的积累,反过来又可以充当信号分子,进一步加剧炎症反应。免疫代谢的重编程影响免疫细胞的功能,对 RA 的发病机制至关重要。此外,线粒体功能障碍在 RA 的糖酵解重编程中起关键作用。这些代谢变化可能是 RA 的潜在治疗靶点。因此,我们回顾了 RA 免疫细胞和成纤维细胞样滑膜细胞 (FLS) 的代谢重编程及其与线粒体功能障碍的关系。

方法

使用 PubMed 数据库和 Web of Science 数据库对已发表的关于免疫代谢重编程、线粒体功能障碍和类风湿性关节炎的文章进行了基于计算机的在线搜索。

结果

本文综述了 RA 中免疫细胞和成纤维细胞样滑膜细胞的代谢重编程及其与线粒体功能障碍的关系,以及与代谢重编程和化疗相关的关键促炎途径,作为未来 RA 的潜在治疗策略。

更新日期:2020-08-14
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