Advancement in understanding the role of ferroptosis in rheumatoid arthritis

Long, Li; Guo, Hongmei; Chen, Xixi; Liu, Yan; Wang, Ruyi; Zheng, Xiaojing; Xiao-bo, Huang; Zhou, Qiao; Wang, Yi

doi:10.3389/fphys.2022.1036515

Cited by 7 publications

(5 citation statements)

References 75 publications

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“…In this study, twelve FRGs were differentially expressed between the synovium of RA patients and HCs. These genes participated in key mechanisms of ferroptosis, including GSH metabolism, iron metabolism and lipid metabolism [ 29 ]. Meanwhile, there were apparent differences in the correlations between FRGs in RA patients and HCs.…”

Section: Discussionmentioning

confidence: 99%

Ferroptosis-Related Molecular Clusters and Diagnostic Model in Rheumatoid Arthritis

Xie

Chen

2023

IJMS

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Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by synovitis, joint damage and deformity. A newly described type of cell death, ferroptosis, has an important role in the pathogenesis of RA. However, the heterogeneity of ferroptosis and its association with the immune microenvironment in RA remain unknown. Synovial tissue samples from 154 RA patients and 32 healthy controls (HCs) were obtained from the Gene Expression Omnibus database. Twelve of twenty-six ferroptosis-related genes (FRGs) were differentially expressed between RA patients and HCs. Furthermore, the patterns of correlation among the FRGs were significantly different between the RA and HC groups. RA patients were classified into two distinct ferroptosis-related clusters, of which cluster 1 had a higher abundance of activated immune cells and a corresponding lower ferroptosis score. Enrichment analysis suggested that tumor necrosis factor-α signaling via nuclear factor-κB was upregulated in cluster 1. RA patients in cluster 1 responded better to anti-tumor necrosis factor (anti-TNF) therapy, which was verified by the GSE 198520 dataset. A diagnostic model to identify RA subtypes and immunity was constructed and verified, in which the area under the curve values in the training (70%) and validation (30%) cohorts were 0.849 and 0.810, respectively. This study demonstrated that there were two ferroptosis clusters in RA synovium that exhibited distinct immune profiles and ferroptosis sensitivity. Additionally, a gene scoring system was constructed to classify individual RA patients.

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Section: Discussionmentioning

confidence: 99%

Ferroptosis-Related Molecular Clusters and Diagnostic Model in Rheumatoid Arthritis

Xie

Chen

2023

IJMS

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“…GPX4 relies on GSH to decrease lipid peroxide. As a critical regulator of ferroptosis, GPX4 is the most potent anti-lipid peroxidase in the cell ( 29 , 30 ). In order to produce GSH, System Xc − is required to exchange extracellular cystine and intracellular glutamate.…”

Section: Core Mechanisms Of Ferroptosismentioning

confidence: 99%

Emerging insights into the role of ferroptosis in the pathogenesis of autoimmune diseases

Fan

Jiang

2023

Front. Immunol.

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Ferroptosis, a novel type of regulated cell death mediated by iron-dependent lipid oxidation, was discovered a decade ago. Significant progress has been made in our knowledge of ferroptosis and immune dysfunction. This review covers recent advancements in the interaction of ferroptosis and the immune system, with an emphasis on autoimmune diseases. The critical regulators of ferroptosis are summarized in the context of reactive oxygen species biology, lipid metabolism, and iron homeostasis. The molecular crosstalk between ferroptosis and different immune cells is also highlighted. Future research is expected to yield new insights into the mechanisms governing ferroptosis and its potential therapeutic benefits in autoimmune diseases.

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“…On the other hand, FLSs produce MMP to digest a variety of proteins in cartilage and supporting structures, further promoting the invasion and expansion of pannus ( 108 ). In addition, VEGF secreted by RA-FLSs is an important factor in promoting angiogenesis ( 109 , 110 ). Thus, it is evident that inducing ferroptosis of RA-FLSs not only regulates synovial homeostasis but also has important implications for the inhibition of angiogenesis.…”

Section: Potential Role Of Ferroptosis In Ra Inflammation and Tissue ...mentioning

confidence: 99%

Ferroptosis as an emerging target in rheumatoid arthritis

Zhao,

Tang,

Wang

et al. 2023

Front. Immunol.

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Rheumatoid arthritis (RA) is an autoimmune disease of unknown etiology. Due to the rise in the incidence rate of RA and the limitations of existing therapies, the search for new treatment strategies for RA has become a global focus. Ferroptosis is a novel programmed cell death characterized by iron-dependent lipid peroxidation, with distinct differences from apoptosis, autophagy, and necrosis. Under the conditions of iron accumulation and the glutathione peroxidase 4 (GPX4) activity loss, the lethal accumulation of lipid peroxide is the direct cause of ferroptosis. Ferroptosis mediates inflammation, oxidative stress, and lipid oxidative damage processes, and also participates in the occurrence and pathological progression of inflammatory joint diseases including RA. This review provides insight into the role and mechanism of ferroptosis in RA and discusses the potential and challenges of ferroptosis as a new therapeutic strategy for RA, with an effort to provide new targets for RA prevention and treatment.

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Advancement in understanding the role of ferroptosis in rheumatoid arthritis

Cited by 7 publications

References 75 publications

Ferroptosis-Related Molecular Clusters and Diagnostic Model in Rheumatoid Arthritis

Ferroptosis-Related Molecular Clusters and Diagnostic Model in Rheumatoid Arthritis

Emerging insights into the role of ferroptosis in the pathogenesis of autoimmune diseases

Ferroptosis as an emerging target in rheumatoid arthritis

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