ArticleBiochemical genetics2026
Association of miR-146a/b and miR-181a with Chronic Obstructive Pulmonary Disease.
Article in Biochemical genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Diagnostic and Monitoring Potential of Sputum-Derived miRNAs in Patients with Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2026Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
miRNAs play critical roles in regulating inflammatory responses in chronic obstructive pulmonary disease (COPD). This study investigated the expression patterns of miR-146a/b and miR-181a, along with associated inflammatory mediators, in COPD patients. This cross-sectional study included 40 patients with acute exacerbation of COPD (AECOPD), 40 patients with stable COPD, and 40 healthy controls. Expression levels of miR-146a, miR-146b, and miR-181a in peripheral blood mononuclear cells (PBMCs) were quantified using quantitative real-time PCR. Serum concentrations of high-mobility group box 1 (HMGB1), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and interleukin-10 (IL-10) were measured by ELISA. Cytokine mRNA expression was assessed in PMA-stimulated PBMCs. Multivariable logistic regression was performed to adjust for potential confounders including age and smoking pack-years. Expression of miR-146a, miR-146b, and miR-181a was significantly decreased in both COPD and AECOPD groups compared to controls (all p < 0.001), with further reduction in AECOPD patients. Multivariable analysis demonstrated that decreased miR-146a (OR = 2.45, 95% CI: 1.58-3.81, p < 0.001) and miR-181a (OR = 2.18, 95% CI: 1.42-3.35, p < 0.001) remained independent predictors of COPD after adjusting for age and smoking exposure. Serum HMGB1, IL-6, and TNF-α levels were significantly elevated in COPD patients, while IL-10 showed decreased expression. PMA-stimulated PBMCs from COPD patients demonstrated enhanced pro-inflammatory cytokine production capacity. In exploratory ROC analysis, miR-146a showed moderate discriminatory capacity (AUC = 0.78, 95% CI: 0.65-0.91). Dysregulation of miR-146a/b and miR-181a is independently associated with COPD, even after accounting for smoking exposure. These findings suggest potential roles in disease pathophysiology, though prospective validation in larger, independent cohorts is required before clinical applicability can be determined.
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Identifiers
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Registered trials
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