滑膜细胞代谢在类风湿关节炎中作用的研究进展
摘要
类风湿关节炎(RA)是一种全身性、难治性、自身免疫性疾病,其主要病理特点是滑膜细胞增生、衬里层增厚、多种炎性细胞浸润、血管翳形成等,这种病理改变是多种因素共同作用的结果。近年来针对RA发生的机制展开了大量的实验研究工作,主要表现在滑膜增生、炎性因子、基因调控等方面。笔者归纳总结了近年来滑膜细胞代谢在RA中作用的研究进展,期望能为RA的治疗提供新模式及新靶点。
引文
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[2] Ferro F,Elefante E,Luciano N,et al.One year in review2017:novelties in the treatment of rheumatoid arthritis[J].Clin Exp Rheumatol,2017,35(5):721-734.
[3] Ganesan R,Rasool M. Fibroblast-like synoviocytes-dependent effector molecules as a critical mediator for rheumatoid arthritis:Current status and future directions[J].Int Rev Immunol,2017,36(1):20-30.
[4] Korb-Pap A,Bertrand J,Sherwood J,et al.Stable activation of fibroblasts in rheumatic arthritis-causes and consequences[J]. Rheumatology(Oxford),2016,55(suppl2):i64-i67.
[5] Takahashi S,Saegusa J,Sendo S,et al. Glutaminase 1plays a key role in the cell growth of fibroblast-like synoviocytes in rheumatoid arthritis[J]. Arthritis Res Ther,2017,19(1):76.
[6] Courtnay R,Ngo DC,Malik N,et al. Cancer metabolism and the Warburg effect:the role of HIF-1 and PI3K[J].Mol Biol Rep,2015,42(4):841-851.
[7] Pearce EL,Poffenberger MC,Chang CH,et al.Fueling immunity:insights into metabolism and lymphocyte function[J].Science,2013,342(6 155):124.
[8] Yang Z,Matteson EL,Goronzy JJ,et al.T-cell metabolism in autoimmune disease[J]. Arthritis Res Ther,2015,17:29.
[9] Matsui T,Nakata N,Nagai S,et al.Inflammatory cytokines and hypoxia contribute to 18F-FDG uptake by cells involved in pannus formation in rheumatoid arthritis[J]. J Nucl Med,2009,50(6):920-926.
[10] Volchenkov R,Dung CM,Elgstoen KB,et al. Metabolic profiling of synovial tissue shows altered glucose and choline metabolism in rheumatoid arthritis samples[J].Scand J Rheumatol,2017,46(2):160-161.
[11] Young SP,Kapoor SR,Viant MR,et al.The impact of inflammation on metabolomic profiles in patients with arthritis[J].Arthritis Rheum,2013,65(8):2 015-2 023.
[12] Zhao Y,Yan X,Li X,et al.PGK1,a glucose metabolism enzyme,may play an important role in rheumatoid arthritis[J].Inflamm Res,2016,65(10):815-825.
[13] Garcia-Carbonell R,Divakaruni AS,Lodi A,et al.Critical Role of Glucose Metabolism in Rheumatoid Arthritis Fibroblast-like Synoviocytes[J]. Arthritis Rheumatol,2016,68(7):1 614-1 626.
[14] Abboud G,Choi SC,Kanda N,et al.Inhibition of Glycolysis Reduces Disease Severity in an Autoimmune Model of Rheumatoid Arthritis[J]. Front Immunol,2018,9:1 973.
[15] Zou Y,Zeng S,Huang M,et al.Inhibition of 6-phosphofructo-2-kinase suppresses fibroblast-like synoviocytes-mediated synovial inflammation and joint destruction in rheumatoid arthritis[J].Br J Pharmacol,2017,174(9):893-908.
[16] Tanaka K,Sasayama T,Irino Y,et al.Compensatory glutamine metabolism promotes glioblastoma resistance to m TOR inhibitor treatment[J]. J Clin Invest,2015,125(4):1 591-1 602.
[17] Guma M,Sanchez-Lopez E,Lodi A,et al.Choline kinase inhibition in rheumatoid arthritis[J]. Ann Rheum Dis,2015,74(7):1 399-1 407.
[18] Li Z,Wu G,van der Veen JN,et al.Phosphatidylcholine metabolism and choline kinase in human osteoblasts[J].Biochim Biophys Acta,2014,1 841(6):859-867.
[19] Mori N,Gadiya M,Wildes F,et al. Characterization of choline kinase in human endothelial cells[J]. NMR Biomed,2013,26(11):1 501-1 507.
[20] Li M,Peng Z,Liu Q,et al.Value of 11C-choline PET/CT for lung cancer diagnosis and the relation between choline metabolism and proliferation of cancer cells[J].Oncol Rep,2013,29(1):205-211.
[21] Friday SC,Fox DA. Phospholipase D enzymes facilitate IL-17-and TNFalpha-induced expression of proinflammatory genes in rheumatoid arthritis synovial fibroblasts(RASF)[J].Immunol Lett,2016,174:9-18.
[22] Baker DA,Eudaly J,Smith CD,et al.Impact of sphingosine kinase 2 deficiency on the development of TNF-alpha-induced inflammatory arthritis[J]. Rheumatol Int,2013,33(10):2 677-2 681.
[23] Gonzalez-Cabrera PJ,Brown S,Studer SM,et al. S1P signaling:new therapies and opportunities[J].F1000Prime Rep,2014,6:109.
[24] Kitano M,Hla T,Sekiguchi M,et al.Sphingosine 1-phosphate/sphingosine 1-phosphate receptor 1 signaling in rheumatoid synovium:regulation of synovial proliferation and inflammatory gene expression[J]. Arthritis Rheum,2006,54(3):742-753.
[25] Kosinska MK,Liebisch G,Lochnit G,et al.Sphingolipids in human synovial fluid——a lipidomic study[J]. PLoS One,2014,9(3):e91 769.
[26] Hutami IR,Izawa T,Mino-Oka A,et al. Fas/S1P1crosstalk via NF-kappa B activation in osteoclasts controls subchondral bone remodeling in murine TMJ arthritis[J]. Biochem Biophys Res Commun,2017,490(4):1 274-1 281.
[27] Bouchareychas L,Grossinger EM,Kang M,et al.Critical Role of LTB4/BLT1 in IL-23-Induced Synovial Inflammation and Osteoclastogenesis via NF-kappa B[J].J Immunol,2017,198(1):452-460.
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[29] Chen M,Lam BK,Luster AD,et al.Joint tissues amplify inflammation and alter their invasive behavior via leukotriene B4 in experimental inflammatory arthritis[J].J Immunol,2010,185(9):5 503-5 511.
[30] Miyabe Y,Miyabe C,Murooka TT,et al.Complement C5a Receptor is the Key Initiator of Neutrophil Adhesion Igniting Immune Complex-induced Arthritis[J]. Sci Immunol,2017,2(7).
[31] Dixit N,Wu DJ,Belgacem YH,et al.Leukotriene B4 activates intracellular calcium and augments human osteoclastogenesis[J].Arthritis Res Ther,2014,16(6):496.
[32] Bouchareychas L,Grossinger EM,Kang M,et al.Critical Role of LTB4/BLT1 in IL-23-Induced Synovial Inflammation and Osteoclastogenesis via NF-kappa B[J].J Immunol,2017,198(1):452-460.
[33] Frommer KW,Schaffler A,Rehart S,et al. Free fatty acids:potential proinflammatory mediators in rheumatic diseases[J].Ann Rheum Dis,2015,74(1):303-310.
[34] Yeom M,Hahm DH,Sur BJ,et al.Phosphatidylserine inhibits inflammatory responses in interleukin-1beta-stimulated fibroblast-like synoviocytes and alleviates carrageenan-induced arthritis in rat[J]. Nutr Res,2013,33(3):242-250.
[35] Rocha DM,Caldas AP,Oliveira LL,et al.Saturated fatty acids trigger TLR4-mediated inflammatory response[J].Atherosclerosis,2016,244:211-215.
[36] Hwang DH,Kim JA,Lee JY.Mechanisms for the activation of Toll-like receptor 2/4 by saturated fatty acids and inhibition by docosahexaenoic acid[J]. Eur J Pharmacol,2016,785:24-35.
[37] Tang MW,Koopman FA,Visscher JP,et al. Hormone,metabolic peptide,and nutrient levels in the earliest phases of rheumatoid arthritis-contribution of free fatty acids to an increased cardiovascular risk during very early disease[J]. Clin Rheumatol,2017,36(2):269-278.
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[39] Guma M,Tiziani S,Firestein GS.Metabolomics in rheumatic diseases:desperately seeking biomarkers[J]. Nat Rev Rheumatol,2016,12(5):269-281.