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类风湿性关节炎(RA)是一种以关节滑膜慢性炎症为主要特征的难治性自身免疫性疾病。高迁移率族蛋白1(HMGB1)是一种染色体结合蛋白,在致病因子刺激下可释放至胞外成为炎症因子诱发炎症反应。HMGB1在RA中起重要作用,通过与相应受体如Toll样受体2(TLR2)、TLR4等结合后启动炎症反应链,可促使巨噬细胞分泌炎性因子,导致关节软骨破坏;同时,HMGB1可促使缺氧诱导因子1α(HIF-1α)、血管内皮生长因子等表达升高,造成血管翳形成,加重关节滑膜的炎性增生;另外,其可增强增生的滑膜组织侵袭能力,进一步造成损伤。因此,HMGB1及其受体通路在当前RA诊疗研究领域日渐受到重视。本文总结了近年来RA研究中HMGB1的致病机制以及其治疗研究进展。
Rheumatoid arthritis (RA) is a refractory autoimmune disease characterized by chronic synovial inflammation. High mobility group box 1 (HMGB1) is a chromosomal binding protein that is released into the extracellular matrix as an inflammatory cytokine-induced inflammatory reaction when stimulated by pathogenic factors. HMGB1 plays an important role in RA. Activation of the inflammatory response chain by binding to corresponding receptors such as Toll-like receptor 2 (TLR2), TLR4 and the like can promote the secretion of inflammatory cytokines by macrophages and cause the destruction of articular cartilage. At the same time, HMGB1 Can promote hypoxia-inducible factor 1α (HIF-1α), vascular endothelial growth factor expression increased, resulting in angiogenesis, increased synovial inflammatory hyperplasia; In addition, it can enhance the proliferation of synovial tissue invasion ability, and further Cause damage. Therefore, HMGB1 and its receptor pathway are gaining more and more attention in the field of current RA diagnosis and treatment. This article summarizes the pathogenesis of HMGB1 in RA and its progress in the treatment of RA in recent years.