ArticleTobacco induced diseases2026
Association of MiR-27a-5p with chronic obstructive pulmonary disease and its role in human bronchial epithelial cell injury: A case-control and in vitro experimental study.
Article in Tobacco induced diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
introductionChronic obstructive pulmonary disease (COPD) lacks effective early diagnostic biomarkers, and the role of miR-27a-5p in COPD pathogenesis remains unclear. This study aimed to explore its inflammatory regulatory mechanism.
methodsWe enrolled COPD patients and healthy controls, measuring miR-27a-5p and inflammatory cytokines (TNF-α, IL-6, IL-1β) in serum and bronchoalveolar lavage fluid. Multivariate logistic regression and ROC curves were used to analyze disease association and diagnostic efficacy. A cigarette smoke extract-induced bronchial epithelial cell model was used with miRNA transfection and dual-luciferase assays to validate the target gene and mechanism.
resultsMiR-27a-5p was significantly upregulated in COPD patients (p<0.001), and its expression was associated with COPD alongside smoking status and pulmonary function (adjusted odds ratio, AOR=22.53; 95% CI: 12.31-41.30, p<0.001). It showed strong diagnostic efficacy (AUC=0.96; 95% CI: 0.92-0.99). In vitro, miR-27a-5p overexpression exacerbated inflammation, while inhibition alleviated it. Mechanistically, miR-27a-5p directly targeted ABL2 to regulate inflammatory cytokine release.
conclusionsMiR-27a-5p within our study was identified as a promising biomarker for COPD susceptibility and modulated airway inflammation via the miR-27a-5p-ABL2 axis.
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