ArticleExperimental and therapeutic medicine2022
Blood CDC42 overexpression is associated with an increased risk of acute exacerbation, inflammation and disease severity in patients with chronic obstructive pulmonary disease.
Article in Experimental and therapeutic medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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Who cites it
2 citing papers in PubMed, 2 citations in OpenAlex.
- FOXD2-AS1/miR-185-5p/CDC42 axis in chronic obstructive pulmonary disease: clinical significance and mechanistic insights.Journal of inflammation (London, England) · 2026Article
- Targeting CDC42 Protects Mitochondrial Function through KLF2/HIF-1α/PINK1 Signaling in Acute Kidney Injury.International journal of biological sciences · 2026Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been previously reported that cell division control 42 (CDC42) protein can regulate macrophage recruitment, T cell-associated inflammation and lung injury. However, its role in chronic obstructive pulmonary disease (COPD) remain poorly understood. Therefore, the present study aimed to investigate the possible association among CDC42 expression, the risk of acute exacerbation and disease features in patients with COPD. Peripheral blood mononuclear cells (PBMCs) and serum samples were collected from 60 patients with acute exacerbation COPD (AE-COPD), 60 patients with stable COPD (S-COPD) and 60 healthy control (HCs) individuals. The mRNA expression levels of CDC42 in PBMCs were then measured using reverse transcription-quantitative PCR. The serum levels of TNF-α, IL-1β, IL-6 and IL-17 were measured using ELISA. The results showed that the expression of CDC42 was dysregulated among patients with AE-COPD and S-COPD compared with that in HCs. Specifically, the expression level of CDC42 was the highest in patients with AE-COPD, followed by those with S-COPD and the lowest in HCs (P<0.001). Furthermore, receiver operating characteristic curve analysis demonstrated that CDC42 expression was associated with an increased risk of acute exacerbation in COPD with an area under curve of 0.690 (95% confidence interval=0.595-0.785). CDC42 was found to be positively associated with Global Initiative for Chronic Obstructive Lung Disease staging in patients with AE-COPD (P<0.01) and S-COPD (P<0.05). Additionally, CDC42 expression associated positively with the serum levels of TNF-α, IL-1β, IL-6 and IL-17 in patients with AE-COPD (all P<0.05). However, this association was weaker in patients with S-COPD and became negligible in HCs. In conclusion, data from the present study suggest that CDC42 is associated with an increased risk of acute exacerbation, inflammation and disease severity in patients with COPD, implicating its application as a potential biomarker for COPD.
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