Ferroptosis in inflammatory arthritis: A promising future

Chang, Siyuan; Tang, Mengshi; Zhang, Bikui; Xiang, Da‐Xiong; Li, Fen

doi:10.3389/fimmu.2022.955069

Cited by 42 publications

(30 citation statements)

References 89 publications

(147 reference statements)

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“…Being an important process in inflammatory diseases (Keuters et al, 2021;Chang et al, 2022), ferroptosis-based strategies have presented a long-time challenge for the clinical development of OA. In a rat OA model, treatment with interleukin (IL)-1β resulted in the decrease of collagen II and GPX4 and an increase in matrix metalloproteinases (MMPs), ROS and ion concentration, contributing to extracellular matrix (ECM) degradation and ferroptosis sensitivity (Lv et al, 2022).…”

Section: Osteoarthritismentioning

confidence: 99%

Current insights into the functional roles of ferroptosis in musculoskeletal diseases and therapeutic implications

Zhang

Yan

Cai

et al. 2023

Front. Cell Dev. Biol.

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Ferroptosis is a novel type of cell death associated with iron accumulation and excessive lipid peroxidation. Elucidating the underlying molecular mechanisms of ferroptosis is intensively related to the development and treatment of multiple diseases, including musculoskeletal disorders. Moreover, in vitro and in vivo studies have shown the importance of oxidative stress in musculoskeletal conditions such as osteoporosis, osteoarthritis, rheumatoid arthritis, and osteosarcoma. Ferroptosis-derived clinical management of musculoskeletal diseases offers tremendous and attractive opportunities. Notably, ferroptosis agonists have been proven to enhance the sensitivity of osteosarcoma cells to conventional therapeutic strategies. In this review, we have mainly focused on the implications of ferroptosis regulation in the pathophysiology and therapeutic response of musculoskeletal disorders. Understanding roles of ferroptosis for controlling musculoskeletal diseases might provide directions for ferroptosis-driven therapies, which could be promising for the development of novel therapeutic strategies.

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Section: Osteoarthritismentioning

confidence: 99%

Current insights into the functional roles of ferroptosis in musculoskeletal diseases and therapeutic implications

Zhang

Yan

Cai

et al. 2023

Front. Cell Dev. Biol.

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“…Previous studies have highlighted the correlation between iron metabolism and chronic anemia in RA patients ( Stefanova et al, 2018 ; Zhao et al, 2022b ; Chang et al, 2022 ). Recently, some studies have shown the involvement of iron metabolism in ferroptosis in RA pathogenies.…”

Section: Ferroptosis and Rheumatoid Arthritismentioning

confidence: 99%

“…This suggests that NR1D1 can potentially be used as therapeutics in the treatment of patients with RA. Various studies have indicated that ROS could be a new therapeutic target for RA treatment regarding ferroptosis ( Xie et al, 2016 ; Xie et al, 2021 ; Chang et al, 2022 ; Lai et al, 2022 ).…”

Section: Use Of Ferroptosis-related Drugs In Rheumatoid Arthritis Tre...mentioning

confidence: 99%

Advancement in understanding the role of ferroptosis in rheumatoid arthritis

et al. 2022

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Rheumatoid arthritis (RA) is a chronic, systemic disease of unknown etiology. The primary manifestation of RA is inflammatory synovitis, which eventually leads to deformity and functional loss. Ferroptosis is a non-apoptosis form of cell death that depends on intracellular iron accumulation. This leads to an increase in reactive oxygen species (ROS) induced-lipid peroxidation. The underlying mechanisms of ferroptosis are System Xc- and Glutathione metabolism, regulation of glutathione peroxidase 4 activity, and ROS generation. Recent studies have shown an association between the pathogenesis of RA and ferroptosis, suggesting the involvement of ferroptosis in the onset and progression of RA. In this review, we have focused on the mechanism of ferroptosis and its association with RA pathogenesis. Further, we discuss the status of therapeutics targeting ferroptosis in the treatment of patients with RA. Targeting ferroptosis could be a potential therapeutic approach for RA treatment.

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“…In addition, increased levels of oxidized protein products (AOPPs) and ROS in serum of AS patients have been found to induce mesenchymal stem cells (MSCs) mitochondrial dysfunction in vitro (23). These evidence of oxidative stress and mitochondrial dysfunction in AS patients inform the existence of ferroptosis in AS (18). These studies indicate that iron homeostasis is involved in the pathogenesis of AS, and the study of the correlation between the two is of potential value for the study of the mechanism and prevention of AS.…”

Section: Introductionmentioning

confidence: 95%

No evidence of a genetic causal relationship between ankylosing spondylitis and iron homeostasis: A two-sample Mendelian randomization study

Yang

et al. 2023

Front. Nutr.

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BackgroundAnkylosing spondylitis (AS) is an immune-mediated chronic inflammatory disease that leads to bone hyperplasia and spinal ankylosis. Iron homeostasis plays a very important role in the inflammatory response and is closely related to the pathogenesis of AS. This study aimed to use large-scale genome-wide association study (GWAS) summary data to study the genetic causal relationship between AS and iron homeostasis using Mendelian randomization (MR).MethodsGenome-wide association study summary data of AS and iron homeostasis-related indicators were obtained from the FinnGen consortium and the DeCODE genetics database, respectively. We used four iron homeostasis-related indicators: ferritin, serum iron, total iron binding capacity (TIBC), and transferrin saturation (TSAT) for two-sample MR analyses to test for genetic causal association with AS using the “TwoSampleMR” package of the R software (version 4.1.2). The random-effects inverse variance weighted (IVW) method was the main analysis method used for MR. We examined the MR analysis results for heterogeneity, horizontal pleiotropy, and possible outliers. In addition, we confirmed the robustness of the MR analysis by testing whether the results were affected by a single SNP and whether they followed a normal distribution.ResultsThe random-effects IVW results showed that ferritin [p = 0.225, OR 95% confidence interval (CI) = 0.836 (0.627–1.116)], serum iron [p = 0.714, OR 95% CI = 0.948 (0.714–1.260)], TIBC [p = 0.380, OR 95% CI = 0.917 (0.755–1.113)], and TSAT [p = 0.674, OR 95% CI = 0.942 (0.713–1.244)] have no genetic causal relationship with AS. We detected no heterogeneity，horizontal pleiotropy and possible outliers in our MR analysis (p > 0.05). In addition, our MR analysis results were not affected by a single SNP, and were normally distributed.ConclusionOur study did not detect a genetic causal relationship between AS and iron homeostasis. Nonetheless, this does not rule out a relationship between the two at other mechanistic levels.

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Ferroptosis in inflammatory arthritis: A promising future

Cited by 42 publications

References 89 publications

Current insights into the functional roles of ferroptosis in musculoskeletal diseases and therapeutic implications

Current insights into the functional roles of ferroptosis in musculoskeletal diseases and therapeutic implications

Advancement in understanding the role of ferroptosis in rheumatoid arthritis

No evidence of a genetic causal relationship between ankylosing spondylitis and iron homeostasis: A two-sample Mendelian randomization study

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