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
来源：
CLINICAL AND EXPERIMENTAL MEDICINE | 2025年 / 25卷 / 01期
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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  • [1] Qiao L., Xu C., Li Q., Mei Z., Li X., Cai H., Et al., Photodynamic therapy activated STAT3 associated pathways: Targeting intrinsic apoptotic pathways to increase PDT efficacy in human squamous carcinoma cells, Photodiagn Photodyn Ther, 14, pp. 119-127, (2016)
  • [2] Lin Y.J., Anzaghe M., Schulke S., Update on the pathomechanism, diagnosis, and treatment options for rheumatoid arthritis, Cells, 9, 4, (2020)
  • [3] Araki Y., Tsuzuki Wada T., Aizaki Y., Sato K., Yokota K., Fujimoto K., Et al., Histone Methylation and STAT-3 Differentially Regulate Interleukin-6-Induced Matrix Metalloproteinase Gene Activation in Rheumatoid Arthritis Synovial Fibroblasts, Arthrit Rheumatol (Hoboken, NJ), 68, 5, pp. 1111-1123, (2016)
  • [4] Tsaltskan V., Firestein G.S., Targeting fibroblast-like synoviocytes in rheumatoid arthritis, Curr Opin Pharmacol, 67, (2022)
  • [5] Smith M.H., Gao V.R., Periyakoil P.K., Kochen A., DiCarlo E.F., Goodman S.M., Et al., Drivers of heterogeneity in synovial fibroblasts in rheumatoid arthritis, Nat Immunol, 24, 7, pp. 1200-1210, (2023)
  • [6] Valencia X., Higgins J.M., Kiener H.P., Lee D.M., Podrebarac T.A., Dascher C.C., Et al., Cadherin-11 provides specific cellular adhesion between fibroblast-like synoviocytes, J Exp Med, 200, 12, pp. 1673-1679, (2004)
  • [7] Wu Z., Ma D., Yang H., Gao J., Zhang G., Xu K., Et al., Fibroblast-like synoviocytes in rheumatoid arthritis: Surface markers and phenotypes, Int Immunopharmacol, 93, (2021)
  • [8] Nygaard G., Firestein G.S., Restoring synovial homeostasis in rheumatoid arthritis by targeting fibroblast-like synoviocytes, Nat Rev Rheumatol, 16, 6, pp. 316-333, (2020)
  • [9] Bartok B., Firestein G.S., Fibroblast-like synoviocytes: key effector cells in rheumatoid arthritis, Immunol Rev, 233, 1, pp. 233-255, (2010)
  • [10] Li C.-C., Zhang Y.-Q., Li W.-J., Mao X., Liu Y.-D., Ma Z.-C., Et al., Exploring the effect and mechanism of Baihu-Guizhi decoction on rheumatoid arthritis with hot syndrome from the angiogenesis regulatory network mediated by VEGF/VEGFR2/PI3K/AKT signaling pathway, (2022)
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