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Published in: Inflammation Research 11/2020

01-11-2020 | Rheumatoid Arthritis | Review

Metabolic reprogramming as a key regulator in the pathogenesis of rheumatoid arthritis

Authors: Wei-wei Cai, Yun Yu, Shi-ye Zong, Fang Wei

Published in: Inflammation Research | Issue 11/2020

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Abstract

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.
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Metadata
Title
Metabolic reprogramming as a key regulator in the pathogenesis of rheumatoid arthritis
Authors
Wei-wei Cai
Yun Yu
Shi-ye Zong
Fang Wei
Publication date
01-11-2020
Publisher
Springer International Publishing
Published in
Inflammation Research / Issue 11/2020
Print ISSN: 1023-3830
Electronic ISSN: 1420-908X
DOI
https://doi.org/10.1007/s00011-020-01391-5

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