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MIF, a potential therapeutic target for rheumatoid arthritis?

作者信息

Chen Zhaolin, Ma Taotao, Huang Cheng, Zhang Lei, Hu Tingting, Li Jun

机构信息

School of Pharmacy, Institute for Liver Diseases of Anhui Medical University (AMU), Anhui Key Laboratory of Bioactivity of Natural Products, Anhui Medical University, Hefei, 230032, China.

出版信息

Rheumatol Int. 2014 Oct;34(10):1481-2. doi: 10.1007/s00296-013-2877-y. Epub 2014 Jan 25.

DOI:10.1007/s00296-013-2877-y
PMID:24463567
Abstract
摘要

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1
MIF, a potential therapeutic target for rheumatoid arthritis?巨噬细胞移动抑制因子，类风湿关节炎的潜在治疗靶点？
Rheumatol Int. 2014 Oct;34(10):1481-2. doi: 10.1007/s00296-013-2877-y. Epub 2014 Jan 25.
2
Macrophage migration inhibitory factor, MIF alleles, and the genetics of inflammatory disorders: incorporating disease outcome into the definition of phenotype.巨噬细胞移动抑制因子、MIF等位基因与炎症性疾病的遗传学：将疾病转归纳入表型定义
Arthritis Rheum. 2003 May;48(5):1171-6. doi: 10.1002/art.10880.
3
Macrophage migration inhibitory factor: a potential therapeutic target for rheumatoid arthritis.巨噬细胞移动抑制因子：类风湿关节炎的潜在治疗靶点。
Korean J Intern Med. 2016 Jul;31(4):634-42. doi: 10.3904/kjim.2016.098. Epub 2016 May 12.
4
Macrophage migration inhibitory factor (MIF) as a therapeutic target for rheumatoid arthritis and systemic lupus erythematosus.巨噬细胞移动抑制因子（MIF）作为类风湿关节炎和系统性红斑狼疮的治疗靶点。
Expert Opin Ther Targets. 2019 Sep;23(9):733-744. doi: 10.1080/14728222.2019.1656718. Epub 2019 Aug 20.
5
Macrophage migration inhibitory factor promoter polymorphisms are associated with disease activity in rheumatoid arthritis patients from Southern Mexico.巨噬细胞移动抑制因子启动子多态性与来自墨西哥南部的类风湿关节炎患者的疾病活动相关。
Mol Genet Genomic Med. 2020 Jan;8(1):e1037. doi: 10.1002/mgg3.1037. Epub 2019 Nov 7.
6
MIF: a new cytokine link between rheumatoid arthritis and atherosclerosis.巨噬细胞移动抑制因子：类风湿关节炎与动脉粥样硬化之间新的细胞因子联系
Nat Rev Drug Discov. 2006 May;5(5):399-410. doi: 10.1038/nrd2029.
7
Macrophage migration inhibitory factor: a key cytokine in RA, SLE and atherosclerosis.巨噬细胞移动抑制因子：类风湿关节炎、系统性红斑狼疮和动脉粥样硬化中的关键细胞因子。
Clin Chim Acta. 2009 Jan;399(1-2):1-7. doi: 10.1016/j.cca.2008.09.014. Epub 2008 Sep 21.
8
Macrophage migration inhibitory factor polymorphisms do not predict therapeutic response to glucocorticoids or to tumour necrosis factor alpha-neutralising treatments in rheumatoid arthritis.巨噬细胞移动抑制因子基因多态性不能预测类风湿关节炎患者对糖皮质激素或肿瘤坏死因子α中和治疗的反应。
Ann Rheum Dis. 2007 Nov;66(11):1525-30. doi: 10.1136/ard.2006.064394. Epub 2007 Apr 24.
9
A functional promoter polymorphism in the macrophage migration inhibitory factor (MIF) gene associated with disease severity in rheumatoid arthritis.巨噬细胞移动抑制因子（MIF）基因中的一个功能性启动子多态性与类风湿关节炎的疾病严重程度相关。
Genes Immun. 2002 May;3(3):170-6. doi: 10.1038/sj.gene.6363867.
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Macrophage migration inhibitory factor upregulates angiogenic factors and correlates with clinical measures in rheumatoid arthritis.巨噬细胞移动抑制因子上调血管生成因子并与类风湿性关节炎的临床指标相关。
J Rheumatol. 2007 May;34(5):927-36. Epub 2007 Apr 1.

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Glycyrrhizin mitigates inflammatory bone loss and promotes expression of senescence-protective sirtuins in an aging mouse model of periprosthetic osteolysis.甘草酸减轻假体周围溶骨症衰老模型中的炎症性骨丢失并促进衰老保护 Sirtuins 的表达。
Biomed Pharmacother. 2021 Jun;138:111503. doi: 10.1016/j.biopha.2021.111503. Epub 2021 Mar 23.
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K/BxN Serum-Transfer Arthritis as a Model for Human Inflammatory Arthritis.K/BxN血清转移关节炎作为人类炎性关节炎的模型
Front Immunol. 2016 Jun 2;7:213. doi: 10.3389/fimmu.2016.00213. eCollection 2016.
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Macrophage Migration Inhibitory Factor (MIF) Supports Homing of Osteoclast Precursors to Peripheral Osteolytic Lesions.

本文引用的文献

1
Macrophage-derived, macrophage migration inhibitory factor (MIF) is necessary to induce disease in the K/BxN serum-induced model of arthritis.巨噬细胞衍生的巨噬细胞移动抑制因子 (MIF) 对于诱导 K/BxN 血清诱导的关节炎模型中的疾病是必要的。
Rheumatol Int. 2013 Sep;33(9):2301-8. doi: 10.1007/s00296-013-2713-4. Epub 2013 Mar 17.
2
Anti-TNF therapy reduces serum levels of chemerin in rheumatoid arthritis: a new mechanism by which anti-TNF might reduce inflammation.抗 TNF 治疗可降低类风湿关节炎患者血清趋化素水平：抗 TNF 可能降低炎症的新机制。
PLoS One. 2013;8(2):e57802. doi: 10.1371/journal.pone.0057802. Epub 2013 Feb 27.
3
巨噬细胞迁移抑制因子（MIF）支持破骨细胞前体归巢至外周溶骨性病变部位。
J Bone Miner Res. 2016 Sep;31(9):1688-700. doi: 10.1002/jbmr.2854. Epub 2016 Jun 2.
Macrophage migration inhibitory factor (MIF): genetic evidence for participation in early onset and early stage rheumatoid arthritis.
巨噬细胞移动抑制因子（MIF）：参与早发性和早期类风湿关节炎的遗传证据。
Cytokine. 2013 Mar;61(3):759-65. doi: 10.1016/j.cyto.2012.12.032. Epub 2013 Feb 9.
4
Influence of MIF, CD40, and CD226 polymorphisms on risk of rheumatoid arthritis.MIF、CD40 和 CD226 多态性对类风湿关节炎风险的影响。
Mol Biol Rep. 2012 Jun;39(6):6915-22. doi: 10.1007/s11033-012-1518-y.
5
Elevated serum levels of macrophage migration inhibitory factor and their significant correlation with rheumatoid vasculitis disease activity.血清巨噬细胞移动抑制因子水平升高及其与类风湿性血管炎疾病活动的显著相关性。
Mod Rheumatol. 2012 Feb;22(1):59-65. doi: 10.1007/s10165-011-0466-z. Epub 2011 May 24.
6
Serum levels of macrophage migration inhibitory factor are associated with rheumatoid arthritis course.巨噬细胞移动抑制因子的血清水平与类风湿关节炎的病程相关。
Rheumatol Int. 2012 Aug;32(8):2307-11. doi: 10.1007/s00296-011-1951-6. Epub 2011 May 24.
7
Macrophage migration inhibitory factor enhances osteoclastogenesis through upregulation of RANKL expression from fibroblast-like synoviocytes in patients with rheumatoid arthritis.巨噬细胞移动抑制因子通过上调类风湿关节炎患者成纤维样滑膜细胞中 RANKL 的表达促进破骨细胞生成。
Arthritis Res Ther. 2011 Mar 14;13(2):R43. doi: 10.1186/ar3279.
8
Macrophage migration inhibitory factor in patients with juvenile idiopathic arthritis.青少年特发性关节炎患者体内的巨噬细胞移动抑制因子
Arthritis Rheum. 2002 Jan;46(1):232-7. doi: 10.1002/1529-0131(200201)46:1<232::AID-ART10059>3.0.CO;2-B.
9
Macrophage migration inhibitory factor up-regulates matrix metalloproteinase-9 and -13 in rat osteoblasts. Relevance to intracellular signaling pathways.巨噬细胞移动抑制因子上调大鼠成骨细胞中的基质金属蛋白酶-9和-13。与细胞内信号通路的相关性。
J Biol Chem. 2002 Mar 8;277(10):7865-74. doi: 10.1074/jbc.M106020200. Epub 2001 Dec 20.
10
Macrophage migration inhibitory factor up-regulates expression of matrix metalloproteinases in synovial fibroblasts of rheumatoid arthritis.巨噬细胞移动抑制因子上调类风湿关节炎滑膜成纤维细胞中基质金属蛋白酶的表达。
J Biol Chem. 2000 Jan 7;275(1):444-50. doi: 10.1074/jbc.275.1.444.