Abstract
Ferroptosis is one of the newly discovered forms of cell-regulated death characterized by iron-dependent lipid peroxidation. Extensive research has focused on the roles of ferroptosis in tumors, blood diseases, and neurological diseases. Some recent findings have indicated that ferroptosis may also be related to the occurrence and development of inflammatory arthritis. Ferroptosis may be a potential therapeutic target, and few studies in vitro and animal models have shown implications in the pathogenesis of inflammatory arthritis. This mini review discussed the common features between ferroptosis and the pathogenesis of rheumatoid arthritis (RA), and evaluated therapeutic applications of ferroptosis regulators in preclinical and clinical research. Some critical issues worth paying attention to were also raised to guide future research efforts.
Highlights
Rheumatoid arthritis (RA) is the most specific systemic immune system disease among autoimmune diseases [1], invading many joints, such as knee and elbow joints
It has been suggested that icariin counteracts the effects of RSL3 on iron content, lipid peroxidation, and relative protein (SLC7A11, SLC3A2L, glutathione peroxidase 4 (GPX4), TRF, nuclear receptor coactivator 4 (NCOA4), and Nrf2) in synoviocytes given the observation that icariin might play a role in protecting synovial cells from ferroptosis [17]
It is worth noting that different cell types may have different susceptibility to ferroptosis
Summary
Rheumatoid arthritis (RA) is the most specific systemic immune system disease among autoimmune diseases [1], invading many joints, such as knee and elbow joints. Its main clinical manifestations are joint swelling and stiffness in the morning. Disease-modifying antirheumatic drugs (DMARDs) are conventional drugs in the treatment of RA. When the disease is refractory, some biologic DMARDs are recommended. The use rate of biological agents in the treatment of RA in North America has been as high as 50.7% [9]. The clinical efficacy rate is inconsistent, ranging from 50% to 70% [10]. We should make changes in the therapeutic strategy when the arthritis is resistant to initial therapy. Different immune cells secrete unique cytokines and jointly stimulate the expression of cytokine
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