目的:呼吸系统疾病(RD)是以肺功能障碍为特征的最常见疾病之一。许多诊断机制已用于鉴定引起RD的病原体。其中,蛋白质组学是一种有价值的诊断方法,用于确定参与RD发病机理的特定蛋白质。因此,在这项研究中,第一次,我们检查了参与慢性阻塞性肺疾病(COPD)发病机理的蛋白质标志物,特发性肺纤维化(IPF),哮喘,闭塞性细支气管炎(BO),和暴露于芥子气的化学战受害者,用蛋白质组学方法进行系统的研究。
方法:直到2023年9月,对几个数据库进行了系统搜索,包括PubMed,Scopus,ISIWebofScience,还有Cochrane.总的来说,根据标准选择4246篇文章进行评估.最后,本系统综述选择了119项研究。
结果:共鉴定出13,806种蛋白质,6471在COPD中,1603在哮喘中,IPF中的5638,三个在BO,91名暴露在芥子气中的受害者。在各种疾病中观察到这些蛋白质表达的改变。经过评估,结果显示,在所有五种疾病中,共有31种蛋白质。
结论:尽管这31种蛋白在所有5种疾病中调节不同的因子和分子通路,它们最终导致炎症途径的调节。换句话说,COPD和芥末暴露患者中某些蛋白质的表达会增加炎症反应,而在IPF,它们会导致肺纤维化。哮喘,由于T细胞向Th2分化而引起过敏反应。
OBJECTIVE: Respiratory disease (RD) is one of the most common diseases characterized by lung dysfunction. Many diagnostic mechanisms have been used to identify the pathogenic agents of responsible for RD. Among these, proteomics emerges as a valuable diagnostic method for pinpointing the specific proteins involved in RD pathogenesis. Therefore, in this study, for the first time, we examined the protein markers involved in the pathogenesis of chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF), asthma, bronchiolitis obliterans (BO), and chemical warfare victims exposed to mustard gas, using the proteomics method as a systematic study.
METHODS: A systematic search was performed up to September 2023 on several databases, including PubMed, Scopus, ISI Web of Science, and Cochrane. In total, selected 4246 articles were for evaluation according to the criteria. Finally, 119 studies were selected for this systematic review.
RESULTS: A total of 13,806 proteins were identified, 6471 in COPD, 1603 in Asthma, 5638 in IPF, three in BO, and 91 in mustard gas exposed victims. Alterations in the expression of these proteins were observed in the respective diseases. After evaluation, the results showed that 31 proteins were found to be shared among all five diseases.
CONCLUSIONS: Although these 31 proteins regulate different factors and molecular pathways in all five diseases, they ultimately lead to the regulation of inflammatory pathways. In other words, the expression of some proteins in COPD and mustard-exposed patients increases inflammatory reactions, while in IPF, they cause lung fibrosis. Asthma, causes allergic reactions due to T-cell differentiation toward Th2.