滑膜在炎性关节病中的作用
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摘要
炎性关节病(IJD)在临床上表现为人体关节和周围组织的炎性反应,对患者的生活质量造成不良影响。除了作为IJD中关节软骨破坏的驱动因素,滑膜炎被学者们认定是骨关节炎中关节软骨变性的重要原因。本文就滑膜的生物学特性、滑膜细胞与IJD的发病关系、内皮细胞与IJD的发病关系进行综述。
引文
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[31] Li J,Hsu HC,Mountz JD. Managing macrophages in rheumatoid arthritis by reform or removal[J]. Curr Rheumatol Rep,2012,14(5):445-454.
[32]温绍君,刘洁琳.血管内皮细胞功能研究概况[J].生殖医学杂志,2005,14(5):310-313.
[33]徐尤年,马璞,张曌,等.内皮细胞的活化/损伤与炎症反应[J].中国急救医学,2010,30(6):552-554.
[34] Ashraf S,Mapp PI,Walsh DA. Angiogenesis and the persistence of inflammation in a rat model of proliferative synovitis[J]. Arthritis Rheum,2010,62(7):1 890-1 898.
[35]李香斌,连金饶,林娜,等.类风湿关节炎滑膜血管生成和血管翳[J].医学综述,2010,16(1):7-9.
[36] Tarrant TK,Patel DD. Chemokines and leukocyte trafficking in rheumatoid arthritis[J]. Pathophysiology,2006,13(1):1-14.
[37] Iwamoto T,Okamoto H,Toyama Y,et al. Molecular aspects of rheumatoid arthritis:chemokines in the joints of patients[J].FEBS J,2008,275(18):4 448-4 455.
[38] Shweiki D,Itin A,Soffer D,et al. Vascular endothelial growth factor induced by hypoxia may mediate hypoxia-initiated angiogenesis[J]. Nature,1992,359(6 398):843-845.
[2]宋朋飞,阚卫兵,袁琴,等.滑膜病变在骨关节炎中的表现[J].中国骨伤,2012,25(5):442-444.
[3] Ai R,Laragione T,Hammaker D,et al. Comprehensive epigenetic landscape of rheumatoid arthritis fibroblast-like synoviocytes[J]. Nat Commun,2018,9(1):1 921.
[4] Tu J,Hong W,Zhang P,et al. Ontology and function of fibroblast-like and macrophage-like synoviocytes:how do they talk to each other and can they be targeted for rheumatoid arthritis therapy?[J]. Front Immunol,2018,9:1 467.
[5]冯小辉.类风湿关节炎滑膜细胞凋亡机制的研究进展[J].医学综述,2013,19(9):1 543-1 545.
[6] Brentano F,Kyburz D,Gay S. Toll-like receptors and rheumatoid arthritis[J]. Methods Mol Biol,2009,517:329-343.
[7]李会丹,李宁丽.滑膜成纤维细胞介导RA关节损伤的免疫学机制[J].现代免疫学,2013,33(6):518-521.
[8] Katsuno Y,Lamouille S,Derynck R. TGF-βsignaling and epithelial-mesenchymal transition in cancer progression[J].Curr Opin Oncol,2013,25(1):76-84.
[9] Asano T,Iwasaki N,Kon S,et al.α9β1 integrin acts as a critical intrinsic regulator of human rheumatoid arthritis[J].Rheumatology(Oxford),2014,53(3):415-424.
[10] Lauzier A,Lavoie RR,Charbonneau M,et al. Snail is a critical mediator of invadosome formation and joint degradation in arthritis[J]. Am J Pathol,2016,186(2):359-374.
[11] Doody KM,Stanford SM,Sacchetti C,et al. Targeting phosphatase-dependent proteoglycan switch for rheumatoid arthritis therapy[J]. Sci Transl Med,2015,7(288):288ra76.
[12]林翊萍,徐沪济.成纤维样滑膜细胞在类风湿关节炎发病机制中的研究进展[J].中华风湿病学杂志,2011,15(1):55-58.
[13]黄英,陈哲,王玉,等.中药对类风湿关节炎成纤维滑膜细胞的影响[J].中华中医药学刊,2017,35(8):2 095-2 097.
[14] Kobayashi T,Okamoto K,Kobata T,et al. Differential regulation of Fas-mediated apoptosis of rheumatoid synoviocytes by tumor necrosis factor alpha and basic fibroblast growth factor is associated with the expression of apoptosis-related molecules[J]. Arthritis Rheum,2000,43(5):1 106-1 114.
[15]彭元洪,钟晓武,青玉凤,等. DNA甲基化在风湿性疾病中的作用研究进展[J].医学综述,2016,22(18):3 557-3 560.
[16] Nakano K,Whitaker JW,Boyle DL,et al. DNA methylome signature in rheumatoid arthritis[J]. Ann Rheum Dis,2013,72(1):110-117.
[17] Karouzakis E,Trenkmann M,Gay RE,et al. Epigenome analysis reveals TBX5 as a novel transcription factor involved in the activation of rheumatoid arthritis synovial fibroblasts[J].J Immunol,2014,193(10):4 945-4 951.
[18]周伟. DNA甲基化对CXCL12/CXCR4生物学轴基因调控的影响及机制[D].济南:山东大学,2009.
[19] Bartholomew B. Regulating the chromatin landscape:structural and mechanistic perspectives[J]. Annu Rev Biochem,2014,83:671-696.
[20] Diermeier S,Kolovos P,Heizinger L,et al. TNFαsignalling primes chromatin for NF-κB binding and induces rapid and widespread nucleosome repositioning[J]. Genome Biol,2014,15(12):536.
[21] Trenkmann M,Brock M,Gay RE,et al. Expression and function of EZH2 in synovial fibroblasts:epigenetic repression of the Wnt inhibitor SFRP1 in rheumatoid arthritis[J]. Ann Rheum Dis,2011,70(8):1 482-1 488.
[22] Hop HT,Reyes AWB,Huy TXN,et al. Activation of NFk B-mediated TNF-induced antimicrobial immunity is required for the efficient brucella abortus clearance in RAW264. 7 cells[J]. Front Cell Infect Microbiol,2017,7:437.
[23] Grabiec AM,Reedquist KA. The ascent of acetylation in the epigenetics of rheumatoid arthritis[J]. Nat Rev Rheumatol,2013,9(5):311-318.
[24] Doody KM,Bottini N,Firestein GS. Epigenetic alterations in rheumatoid arthritis fibroblast-like synoviocytes[J]. Epigenomics,2017,9(4):479-492.
[25] Hawtree S,Muthana M,Wilkinson JM,et al. FRI0360 histone deacetylase one contributes to the auto-aggressive phenotype of rheumatoid arthritis synovial fibroblasts[J]. Ann Rheum Dis,2014,73(Suppl 2):517.
[26] Klein K,Kabala PA,Grabiec AM,et al. The bromodomain protein inhibitor I-BET151 suppresses expression of inflammatory genes and matrix degrading enzymes in rheumatoid arthritis synovial fibroblasts[J]. Ann Rheum Dis,2016,75(2):422-429.
[27]奚正德,葛海良.巨噬细胞及其表达和分泌产物在类风湿性关节炎发病中的作用[J].自然杂志,2009,31(5):262-267.
[28]周琦,刘树民,董婉茹."TLR2/4-NF-κB"信号转导通路在痛风性关节炎发病中的作用机制[J].中国药师,2016,19(9):1 733-1 736.
[29] Zong H,Li X,Lin H,et al. Lipoxin A4 pretreatment mitigates skeletal muscle ischemia-reperfusion injury in rats[J]. Am J Transl Res,2017,9(3):1 139-1 150.
[30] Kennedy A,Fearon U,Veale DJ,et al. Macrophages in synovial inflammation[J]. Front Immunol,2011,2:52.
[31] Li J,Hsu HC,Mountz JD. Managing macrophages in rheumatoid arthritis by reform or removal[J]. Curr Rheumatol Rep,2012,14(5):445-454.
[32]温绍君,刘洁琳.血管内皮细胞功能研究概况[J].生殖医学杂志,2005,14(5):310-313.
[33]徐尤年,马璞,张曌,等.内皮细胞的活化/损伤与炎症反应[J].中国急救医学,2010,30(6):552-554.
[34] Ashraf S,Mapp PI,Walsh DA. Angiogenesis and the persistence of inflammation in a rat model of proliferative synovitis[J]. Arthritis Rheum,2010,62(7):1 890-1 898.
[35]李香斌,连金饶,林娜,等.类风湿关节炎滑膜血管生成和血管翳[J].医学综述,2010,16(1):7-9.
[36] Tarrant TK,Patel DD. Chemokines and leukocyte trafficking in rheumatoid arthritis[J]. Pathophysiology,2006,13(1):1-14.
[37] Iwamoto T,Okamoto H,Toyama Y,et al. Molecular aspects of rheumatoid arthritis:chemokines in the joints of patients[J].FEBS J,2008,275(18):4 448-4 455.
[38] Shweiki D,Itin A,Soffer D,et al. Vascular endothelial growth factor induced by hypoxia may mediate hypoxia-initiated angiogenesis[J]. Nature,1992,359(6 398):843-845.