期刊
FRONTIERS IN IMMUNOLOGY
卷 13, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2022.930278
关键词
rheumatoid arthritis; autoimmune disease; inflammation; cuproptosis; cuproptosis-related genes
类别
资金
- National Natural Science Funds of China [82074234, 82071756]
- National Key Research and Development Project [2018YFC1705200, 2018YFC1705203]
- Shanghai Chinese Medicine Development Office
- National Administration of Traditional Chinese Medicine
- Regional Chinese Medicine (Specialist) Diagnosis and Treatment Center Construction Project-Rheumatology
- State Administration of Traditional Chinese Medicine
- National TCM Evidence-Based Medicine Research and Construction Project
- Basic TCM Evidence-Based Capacity Development Program
- Shanghai Municipal Health Commission
- East China Region-based Chinese and Western Medicine Joint Disease Specialist Alliance
This study explores the link between cuproptosis and the pathological mechanisms of rheumatoid arthritis (RA), as well as its effects on various immune cells. The findings provide a theoretical basis for translating preclinical and experimental results into clinical protocols for RA treatment.
Rheumatoid arthritis (RA) is an autoimmune disease that severely affects patients' physical and mental health, leading to chronic synovitis and destruction of bone joints. Although various available clinical treatment options exist, patients respond with varying efficacies due to multiple factors, and there is an urgent need to discover new treatment options to improve clinical outcomes. Cuproptosis is a newly characterized form of cell death. Copper causes cuproptosis by binding to lipid-acylated components of the tricarboxylic acid cycle, leading to protein aggregation, loss of iron-sulfur cluster proteins, and eventually proteotoxic stress. Targeting copper cytotoxicity and cuproptosis are considered potential options for treating oncological diseases. The synovial hypoxic environment and the presence of excessive glycolysis in multiple cells appear to act as inhibitors of cuproptosis, which can lead to excessive survival and proliferation of multiple immune cells, such as fibroblast-like synoviocytes, effector T cells, and macrophages, further mediating inflammation and bone destruction in RA. Therefore, in this study, we attempted to elaborate and summarize the linkage of cuproptosis and key genes regulating cuproptosis to the pathological mechanisms of RA and their effects on a variety of immune cells. This study aimed to provide a theoretical basis and support for translating preclinical and experimental results of RA to clinical protocols.
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