Metabolic reprogramming as a key regulator in the pathogenesis of rheumatoid arthritis
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Inflammation Research
REVIEW
Metabolic reprogramming as a key regulator in the pathogenesis of rheumatoid arthritis Wei‑wei Cai1 · Yun Yu1 · Shi‑ye Zong1 · Fang Wei1 Received: 15 June 2020 / Revised: 2 August 2020 / Accepted: 5 August 2020 © Springer Nature Switzerland AG 2020
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. Keywords Rheumatoid arthritis · Metabolic reprogramming · Mitochondrial dysfunction · T cells · Macrophages · Fibroblast-like synoviocytes
Introduction Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic, progressive synovitis of the joints [1]. RA is characterized by synovial infiltration by immune cells such as T cells, B cells, and monocytes, and neovascularization. Multiple T-cell subtypes and their respective effectors participate in the pathogenesis of RA by mediating chronic inflammation. Type 1 T-helper cells (Th1) and Type 17 T-helper (Th17) cells are overactivated and secrete pro-inflammatory cytokines and chemokines to promote the pathogenesis of RA [2]. Regulatory T (Treg) cells can Responsible Editor: John Di Battista. * Fang Wei [email protected] 1
School of Pharmacy, Bengbu Medical College, Bengbu 233030, Anhui, China
prevent autoimmunity by inhibiting effector T-cell proliferation and transforming growth factor-β (TGF-β) [1]. Treg cells were consistently detected in the blood and synovial fluid of RA patients [3]. In addition, synovial lining hyperplasia (pannus) caused by proliferation of macrophages and fibroblast-like synovi
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