ArticleInternational journal of chronic obstructive pulmonary disease2020
PTPLAD2 and USP49 Involved in the Pathogenesis of Smoke-Induced COPD by Integrative Bioinformatics Analysis.
Article in International journal of chronic obstructive pulmonary disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
- The interplay between oxidative stress and autophagy in chronic obstructive pulmonary disease.Frontiers in physiology · 2022Pooled it
- Chronic Exposure to Cigarette Smoke Induces Pyroptosis in Pulmonary Epithelial Cells via EGR1/USP44/TRAF6 Axis in COPD.Journal of inflammation research · 2025Article
- The Correlation Analysis Between m6A Methylation Modification and Ferroptosis Induced by Cigarette Smoke in Human Bronchial Epithelium.Immunity, inflammation and disease · 2024Article
- TET2 stabilized by deubiquitinase USP21 ameliorates cigarette smoke-induced apoptosis in airway epithelial cells.iScience · 2024Article
- Copper homeostasis dysregulation in respiratory diseases: a review of current knowledge.Frontiers in physiology · 2024Review
- Identification of Potential Key Genes in the Pathogenesis of Chronic Obstructive Pulmonary Disease Through Bioinformatics Analysis.Frontiers in genetics · 2021Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Chronic obstructive pulmonary disease (COPD) is a typical chronic disease, but its molecular pathogenesis remains unclear. This study aimed to investigate the expression of biomarkers during COPD development. Methods: Markers significantly associated with COPD were screened using bioinformatics tools. qRT-PCR and Western blot were used to explore the expression of PTPLAD2 and USP49 in BEAS-2B cells. CCK-8 assay was used to determine the influence of PTPLAD2 and USP49 in BEAS-2B on cell proliferation. Results: In this study, 86 DEGs were identified in GSE76925. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses suggested that the phosphoinositide 3-kinase-Akt signaling pathway, ECM-receptor interaction, mRNA process, and viral transcription were all involved in the development of COPD. In addition, 14 hub genes were identified by WGCNA. PTPLAD2 and USP49 shared DEGs and hub genes and their expression levels were significantly reduced after CSE-treatment in BEAS-2B cells. Conclusion: Our results suggest that PTPLAD2 and USP49 may be useful biomarkers of COPD.
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Registered trials
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