泛素化与慢性阻塞性肺疾病的研究进展

Research progress of ubiquitination and chronic obstructive pulmonary disease

泛素化是蛋白质最常见的翻译后修饰,是蛋白质降解的信号,细胞内80%以上的蛋白质是通过泛素蛋白酶体系统降解的。泛素化广泛参与细胞各种生命过程。慢性阻塞性肺疾病(COPD)是一种以持续性气流受限为特征的慢性呼吸道炎症性疾病,其发病机制为蛋白酶-抗蛋白酶失衡机制、氧化应激机制及炎症机制。此外,COPD肺组织中自噬增加。相关研究表明,泛素化参与COPD发病机制的各个环节,E3泛素连接酶是TRIM家族的一员,在泛素化过程中发挥重要作用,但与COPD发病是否相关尚未有人报道。本文综述了近几年国内外学者关于泛素化与COPD的研究进展,通过进一步研究COPD的发病机制,以期发现COPD的治疗干预靶点,为临床治疗提供理论依据。

Ubiquitination is the most common post-translational modification of proteins,and it is a signal of protein degradation.More than 80%of proteins in intracellular are degraded through the ubiquitin-proteasome system.Ubiquitination is involved in regulation of a series of cellular life processes.Chronic obstructive pulmonary disease(COPD)is defined as a chronic respiratory inflammatory disease characterized by persistent airflow limitation.Its pathogenesis are proteinase-antiproteinase mechanism,oxidative stress mechanism and inflammatory mechanism.In addition,autophagy increases in pulmonary tissue of COPD.Relevant studies have shown that ubiquitination is involved in various aspects of the pathogenesis of COPD.E3 ubiquitin ligase is a member of TRIM family and plays an important role in the ubiquitination process.However,whether it is related to the pathogenesis of COPD has not been reported.In this paper,the research progress of ubiquitination and COPD by domestic and foreign scholars in recent years was reviewed.Through further study on the pathogenesis of COPD,we hope to find out the therapeutic or intervention targets of COPD,providing theoretical basis for clinical treatment.