The double-edged sword of lncRNAs in rheumatoid arthritis: from controlling the disease to its progress

被引:0
作者
Liu, Zhenyu [1 ]
Xu, Hongbo [2 ]
Chen, Zhihua [3 ]
机构
[1] Yanbian Univ, Med Coll, Dept Tradit Chinese Med, Yanji 133001, Jilin Province, Peoples R China
[2] Yanbian Tradit Chinese Med Hosp, Dept Med, Jilin 133000, Jilin Province, Peoples R China
[3] Yanbian Univ, Nursing Coll, Yanji 133001, Jilin, Peoples R China
关键词
LncRNAs; RA; Inflammatory responses; LONG NONCODING RNA; FIBROBLAST-LIKE SYNOVIOCYTES; CELL-PROLIFERATION; ESTROGEN-RECEPTOR; T-CELLS; ACTIVATION; PROMOTES; MIGRATION; INVASION; EXPRESSION;
D O I
10.1007/s10238-025-01567-5
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by chronic inflammatory responses in the joints, synovial hyperplasia, persistent abnormal proliferation of fibroblast-like synoviocytes (FLSs), and cartilage erosion, leading to joint swelling and destruction. The underlying mechanisms of this disease entail a complex interplay of factors, with long noncoding RNAs (lncRNAs) serving as the main contributors. These lncRNAs, which are over 200 bp in length, are involved in regulating inflammatory responses, joint damage, and FLS growth. Studies have shown that lncRNAs have a dual function in the progression of RA, as they can both promote the disease and control inflammatory responses to reduce symptoms. Nevertheless, our current understanding of the dual function of lncRNAs in the development of RA is incomplete, and the exact molecular mechanisms involved in this process remain unclear. This study aims to elucidate the molecular mechanisms by which lncRNAs exert their inhibitory and stimulatory effects, as well as explore the potential of lncRNAs in diagnosing, predicting the prognosis, and targeting therapy for RA.
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页数:13
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  • [41] Liu Y., Tanabe K., Baronnier D., Patel S., Woodgett J., Cras-Meneur C., Et al., Conditional ablation of Gsk-3β in islet beta cells results in expanded mass and resistance to fat feeding-induced diabetes in mice, Diabetologia, 53, pp. 2600-2610, (2010)
  • [42] Jiang H., Fan C., Lu Y., Cui X., Liu J., Astragaloside regulates lncRNA LOC100912373 and the miR-17-5p/PDK1 axis to inhibit the proliferation of fibroblast-like synoviocytes in rats with rheumatoid arthritis, Int J Mol Med, 48, 1, pp. 1-10, (2021)
  • [43] Zhuo Q., Wei L., Yin X., Li H., Qin G., Li S., Et al., LncRNA ZNF667-AS1 alleviates rheumatoid arthritis by sponging miR-523-3p and inactivating the JAK/STAT signalling pathway, Autoimmunity, 54, 7, pp. 406-414, (2021)
  • [44] Jung Y.K., Kang Y.M., Han S., Osteoclasts in the inflammatory arthritis: implications for pathologic osteolysis, Immune Network, (2019)
  • [45] Song J., Kim D., Han J., Kim Y., Lee M., Jin E.-J., PBMC and exosome-derived Hotair is a critical regulator and potent marker for rheumatoid arthritis, Clin Exp Med, 15, pp. 121-126, (2015)
  • [46] Xie B., Chen S., Xu Y., Han W., Hu R., Chen M., Et al., The impact of glucagon-like peptide 1 receptor agonists on bone metabolism and its possible mechanisms in osteoporosis treatment, Front Pharmacol, 12, (2021)
  • [47] Li W., Zhang B., Zhu H.M., Huang S.M., Xu H.D., CRNDE impacts the proliferation of osteoclast by estrogen deficiency in postmenopausal osteoporosis, European Review for Medical & Pharmacological Sciences, 22, 18, (2018)
  • [48] Xiao S., Ouyang Q., Feng Y., Lu X., Han Y., Ren H., Et al., LncNFYB promotes the proliferation of rheumatoid arthritis fibroblast-like synoviocytes via LncNFYB/ANXA2/ERK1/2 axis, J Biol Chem, 300, 2, (2024)
  • [49] Sun Y., Liu J., Wen J., Huang D., Zhou Q., Zhang X., Et al., Overexpression of long noncoding RNA LINC00638 inhibits inflammation and oxidative stress in rheumatoid arthritis fibroblast-like synoviocytes by regulating the Nrf2/HO-1 pathway, Immun Inflamm Dis, 10, 7, (2022)
  • [50] Su Y., Liu Y., Ma C., Guan C., Ma X., Meng S., Mesenchymal stem cell-originated exosomal lncRNA HAND2-AS1 impairs rheumatoid arthritis fibroblast-like synoviocyte activation through miR-143-3p/TNFAIP3/NF-κB pathway, J Orthop Surg Res, 16, pp. 1-14, (2021)