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Evaluation of common protein biomarkers involved in the pathogenesis of respiratory diseases with proteomic methods: A systematic review

Authors :
Hadi Rezaeeyan
Masoud Arabfard
Hamid R. Rasouli
Alireza Shahriary
B. Fatemeh Nobakht M. Gh
Source :
Immunity, Inflammation and Disease, Vol 11, Iss 11, Pp n/a-n/a (2023)
Publication Year :
2023
Publisher :
Wiley, 2023.

Abstract

Abstract Aim 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. Materials and 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. Conclusion 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.

Details

Language :
English
ISSN :
20504527
Volume :
11
Issue :
11
Database :
Directory of Open Access Journals
Journal :
Immunity, Inflammation and Disease
Publication Type :
Academic Journal
Accession number :
edsdoj.3f5d5eaddd444ef0afd66a3ee1d55057
Document Type :
article
Full Text :
https://doi.org/10.1002/iid3.1090