多发性硬化症的病因涉及多种信号传导途径改变,这就为我们研发更加有效的治疗药物提出了更大挑战。已知在多发性硬化症中多种细胞因子及其受体信号传导异常,根据其下游效应分子不同分为:Jak/Stat,NF-κB,ERK1/2,p38 or Jun/Fos通路等。目前仅有部分多发性硬化症治疗药物靶向上述信号通路,本文将综述系统生物学最新研究成果分别阐述多发性硬化症发生发展过程中信号通路的异常,为今后靶向上述通路的新药研发提供个体化或复合型治疗策略。
The pathogenesis of multiple sclerosis ( MS) involves alterations to multiple pathways and processes, which represent a significant challenge for developing more-effective therapies.In MS, abnormalities have been identified in several cytokine-signaling pathways, as well as those of other immune receptors.Among the downstream molecules implicated are Jak/Stat, NF-κb, ERK1/2, p38 or Jun/Fos, current MS drugs target some of these pathways.This article will with the aid of the latest research results of systems biology approaches that study pathway dysregulation in the process of MS development, targeting these relevant MS-signaling pathways, offers the opportunity to accelerate the development of novel individual or combination therapies for the future of new drug research.