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Role of Myokines in Myositis Pathogenesis and Their Potential to be New Therapeutic Targets in Idiopathic Inflammatory Myopathies.
Journal of Immunology Research ( IF 3.5 ) Pub Date : 2020-07-24 , DOI: 10.1155/2020/9079083
Vlad Mageriu 1, 2 , Emilia Manole 1, 3 , Alexandra E Bastian 4, 5 , Florica Staniceanu 5
Affiliation  

Idiopathic inflammatory myopathies (IIM) represent a heterogeneous group of autoimmune diseases whose treatment is often a challenge. Many patients, even after immunosuppressive therapy, do not respond to treatment, so new alternatives have been sought for this. Therefore, other signaling pathways that could contribute to the pathogenesis of myositis have been investigated, such as the expression of myokines in skeletal muscle in response to the inflammatory process. In this review, we will refer to these muscle cytokines that are overexpressed or downregulated in skeletal muscle in patients with various forms of IIM, thus being able to contribute to the maintenance of the autoimmune process. Some muscle cytokines, through their antagonistic action, may be a helpful contributor to the disease modulation, and thus, they could represent personalized treatment targets. Here, we consider the main myokines involved in the pathogenesis of myositis, expressing our view on the possibility of using them as potential therapeutic targets: interleukins IL-6, IL-15, and IL-18; chemokines CXCL10, CCL2, CCL3, CCL4, CCL5, and CCL20; myostatin; follistatin; decorin; osteonectin; and insulin-like 6. An interesting topic regarding the complex connection between myokines and noninflammatory pathways implied in IIM has also been briefly described, because it is an important scientific approach to the pathogenesis of IIM and can be a therapeutic alternative to be considered, especially for the patients who do not respond to immunosuppressive treatment.

中文翻译:


肌因子在肌炎发病机制中的作用及其成为特发性炎症性肌病新治疗靶点的潜力。



特发性炎症性肌病(IIM)代表一组异质性自身免疫性疾病,其治疗通常是一个挑战。许多患者即使在接受免疫抑制治疗后也对治疗没有反应,因此人们正在寻找新的替代方案。因此,人们已经研究了可能有助于肌炎发病机制的其他信号通路,例如骨骼肌中肌因子对炎症过程的反应的表达。在这篇综述中,我们将提及这些在各种形式的 IIM 患者骨骼肌中过度表达或下调的肌肉细胞因子,从而能够有助于维持自身免疫过程。一些肌肉细胞因子通过其拮抗作用,可能有助于疾病调节,因此,它们可以代表个性化的治疗目标。在这里,我们考虑了参与肌炎发病机制的主要肌因子,表达了我们对将它们作为潜在治疗靶点的可能性的看法:白细胞介素 IL-6、IL-15 和 IL-18;趋化因子 CXCL10、CCL2、CCL3、CCL4、CCL5 和 CCL20;肌肉生长抑制素;卵泡抑素;核心蛋白聚糖;骨连接蛋白;和胰岛素样 6. 还简要描述了关于 IIM 中隐含的肌因子和非炎症途径之间复杂联系的一个有趣主题,因为它是研究 IIM 发病机制的重要科学方法,并且可以作为一种值得考虑的治疗替代方案,特别是适用于对免疫抑制治疗无反应的患者。
更新日期:2020-07-24
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