ArticleImmunity, inflammation and disease2024
Analysis of network expression and immune infiltration of disulfidptosis-related genes in chronic obstructive pulmonary disease.
Article in Immunity, inflammation and disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Exosomal miR-181d-5p derived from distal airway stem cells inhibit apoptosis of pulmonary vascular endothelial cells in COPD mice by targeting PDAP1.Stem cell research & therapy · 2026Article
- Article
- The role of programmed cell death in chronic obstructive pulmonary disease: from pathogenesis to treatment.Frontiers in immunology · 2026Review
- A Novel Disulfidptosis-Related Diagnostic Gene Signature and Differential Expression Validation in Ischaemic Cardiomyopathy.Journal of cellular and molecular medicine · 2025Article
- Immunometabolic regulation of disulfidptosis in orthopedic diseases: mechanistic heterogeneity and therapeutic targets.Frontiers in immunology · 2025Review
- Exploring the diagnostic and immune infiltration roles of disulfidptosis related genes in pulmonary hypertension.Respiratory research · 2024Article
- Analysis of network expression and immune infiltration of disulfidptosis-related genes in chronic obstructive pulmonary disease.Immunity, inflammation and disease · 2024Article
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundChronic obstructive pulmonary disease (COPD) is a globally prevalent respiratory disease, and programmed cell death plays a pivotal role in the development of COPD. Disulfidptosis is a newly discovered type of cell death that may be associated with the progression of COPD. However, the expression and role of disulfidptosis-related genes (DRGs) in COPD remain unclear.
methodsThe expression of DRGs was identified by analyzing RNA sequencing (RNA-seq) data in COPD. Further, COPD patients were classified into two subtypes by unsupervised cluster analysis to reveal their differences in gene expression and immune infiltration. Meanwhile, hub genes associated with disulfidptosis were screened by weighted gene co-expression network analysis. Subsequently, the hub genes were validated experimentally in cells and animals. In addition, we screened potential therapeutic drugs through the hub genes.
resultsWe identified two distinct molecular clusters and observed significant differences in immune cell populations between them. In addition, we screened nine hub genes, and experimental validation showed that CDC71, DOHH, PDAP1, and SLC25A39 were significantly upregulated in cigarette smoke-induced COPD mouse lung tissues and bronchial epithelial cells (BEAS-2B) treated with cigarette smoke extract. Finally, we predicted 10 potential small molecule drugs such as Atovaquone, Taurocholic acid, Latamoxef, and Methotrexate.
conclusionWe highlighted the strong association between COPD and disulfidptosis, with DRGs demonstrating a discriminative capacity for COPD. Additionally, the expression of certain novel genes, including CDC71, DOHH, PDAP1, and SLC25A39, is linked to COPD and may aid in the diagnosis and assessment of this condition.
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