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Indian J Clin Biochem. 2014 Oct;29(4):491-5. doi: 10.1007/s12291-013-0387-z. Epub 2013 Sep 28.
2
Effects of imatinib mesylate in mouse models of multiple sclerosis and in vitro determinants.甲磺酸伊马替尼在多发性硬化症小鼠模型中的作用及体外决定因素。
Iran J Allergy Asthma Immunol. 2014 Jun;13(3):198-206.
3
The significance of matrix metalloproteinases in the immunopathogenesis and treatment of multiple sclerosis.基质金属蛋白酶在多发性硬化症免疫发病机制及治疗中的意义
Sultan Qaboos Univ Med J. 2014 Feb;14(1):e13-25. doi: 10.12816/0003332. Epub 2014 Jan 27.
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Functional switch from pro-neurotrophins to mature neurotrophins.从前神经生长因子向成熟神经生长因子的功能转换。
Curr Protein Pept Sci. 2013 Nov;14(7):617-25. doi: 10.2174/1389203711209070658.
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Imatinib mesylate: an innovation in treatment of autoimmune diseases.甲磺酸伊马替尼:自身免疫性疾病治疗的一项创新。
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The emerging role of p38 mitogen-activated protein kinase in multiple sclerosis and its models.p38 丝裂原活化蛋白激酶在多发性硬化及其模型中的新作用。
Mol Cell Biol. 2013 Oct;33(19):3728-34. doi: 10.1128/MCB.00688-13. Epub 2013 Jul 29.
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Sunitinib enhances neuronal survival in vitro via NF-κB-mediated signaling and expression of cyclooxygenase-2 and inducible nitric oxide synthase.舒尼替尼通过 NF-κB 介导的信号通路和环氧化酶-2 及诱导型一氧化氮合酶的表达增强体外神经元的存活。
J Neuroinflammation. 2013 Jul 23;10:93. doi: 10.1186/1742-2094-10-93.
8
M-CSF increases proliferation and phagocytosis while modulating receptor and transcription factor expression in adult human microglia.M-CSF 可增加成年人类小神经胶质细胞的增殖和吞噬作用,同时调节受体和转录因子的表达。
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9
Imatinib ameliorates neuroinflammation in a rat model of multiple sclerosis by enhancing blood-brain barrier integrity and by modulating the peripheral immune response.伊马替尼通过增强血脑屏障完整性和调节外周免疫反应改善多发性硬化症大鼠模型的神经炎症。
PLoS One. 2013;8(2):e56586. doi: 10.1371/journal.pone.0056586. Epub 2013 Feb 20.
10
EphA4 receptor tyrosine kinase is a modulator of onset and disease severity of experimental autoimmune encephalomyelitis (EAE).EphA4 受体酪氨酸激酶是实验性自身免疫性脑脊髓炎(EAE)发病和疾病严重程度的调节剂。
PLoS One. 2013;8(2):e55948. doi: 10.1371/journal.pone.0055948. Epub 2013 Feb 4.

受体酪氨酸激酶与酪氨酸激酶抑制剂:多发性硬化症治疗成功的新希望

Receptor Tyrosine Kinase and Tyrosine Kinase Inhibitors: New Hope for Success in Multiple Sclerosis Therapy.

作者信息

Mirshafiey Abbas, Ghalamfarsa Ghasem, Asghari Babak, Azizi Gholamreza

机构信息

Dr. Mirshafiey is from the Departmant of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran; Dr. Ghalamfarsa is from Cellular & Molecular Research Center, Yasuj University of Medical Sciences, Yasuj, Iran; Dr. Asghari is from Antimicrobial Resistance Research Center, Faculty of Medicine, Iran University of Medical Science, Tehran, Iran; Dr. Azizi is from Imam Hassan Mojtaba Hospital, Alborz University of Medical Sciences, Karaj, Iran.

出版信息

Innov Clin Neurosci. 2014 Jul;11(7-8):23-36.

PMID:25337443
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4204472/
Abstract

Receptor tyrosine kinases (RTKs) are essential components of signal transduction pathways that mediate cell-to-cell communication and their function as relay points for signaling pathways. They have a key role in numerous processes that control cellular proliferation and differentiation, regulate cell growth and cellular metabolism, and promote cell survival and apoptosis. Recently, the role of RTKs including TCR, FLT-3, c-Kit, c-Fms, PDGFR, ephrin, neurotrophin receptor, and TAM receptor in autoimmune disorder, especially rheumatoid arthritis and multiple sclerosis has been suggested. In multiple sclerosis pathogenesis, RTKs and their tyrosine kinase enzymes are selective important targets for tyrosine kinase inhibitor (TKI) agents. TKIs, compete with the ATP binding site of the catalytic domain of several tyrosine kinases, and act as small molecules that have a favorable safety profile in disease treatment. Up to now, the efficacy of TKIs in numerous animal models of MS has been demonstrated, but application of these drugs in human diseases should be tested in future clinical trials.

摘要

受体酪氨酸激酶(RTKs)是信号转导通路的重要组成部分,介导细胞间通讯,并作为信号通路的中继点发挥作用。它们在控制细胞增殖和分化、调节细胞生长和细胞代谢以及促进细胞存活和凋亡的众多过程中起着关键作用。最近,有人提出包括TCR、FLT-3、c-Kit、c-Fms、PDGFR、ephrin、神经营养因子受体和TAM受体在内的RTKs在自身免疫性疾病,尤其是类风湿性关节炎和多发性硬化症中的作用。在多发性硬化症发病机制中,RTKs及其酪氨酸激酶酶是酪氨酸激酶抑制剂(TKI)药物的选择性重要靶点。TKI与几种酪氨酸激酶催化域的ATP结合位点竞争,并作为在疾病治疗中具有良好安全性的小分子发挥作用。到目前为止,TKI在多种MS动物模型中的疗效已得到证实,但这些药物在人类疾病中的应用应在未来的临床试验中进行测试。