ArticleTobacco induced diseases2025
MicroRNA-21 plays a role in exacerbating chronic obstructive pulmonary disease by regulating necroptosis and apoptosis in bronchial epithelial cells.
Article in Tobacco induced diseases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Sputum Exosomal microRNAs as Non-Invasive Biomarkers in COPD: A Cross-Sectional Study.Biomedicines · 2025Article
- Review
- Exercise and Epigenetic Regulation in COPD: Current Evidence and Potential Mechanistic Pathways.International journal of molecular sciences · 2025Review
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Authors and funding
7 authors.
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Abstract
introductionBronchial epithelial cell damage is an important determinant of the severity of chronic obstructive pulmonary (COPD). However, the exact molecular mechanisms underlying this cell death in COPD development are not well understood. This study investigates the involvement of microRNA-21 (miR-21/miRNA-21) in COPD and its underlying molecular mechanism.
methodsA mouse model of COPD was created by exposing the mice to cigarette smoke (CS) and injecting them with cigarette smoke extract (CSE). Both wild-type mice and miR-21 knockout (miR-21-/-) mice were used to investigate the role of microRNA-21 (miR-21) in exacerbating COPD. Various assays and analyses were performed, including HE staining, tunel staining, enzyme-linked immunosorbent assay (ELISA), flow cytometry, quantitative real-time polymerase chain reaction (RT-qPCR), and western blotting (WB) to measure outcomes such as the pathological morphological changes, necroptosis, apoptosis, and levels of inflammatory factors.
resultsOur results revealed an upregulation of miR-21 in the lung tissue of COPD model mice. Additionally, knockout of miR-21 resulted in decreased levels of bronchial epithelial cell necroptosis and apoptosis, as evidenced by the downregulation of tumor necrosis factor receptor 1 (TNFR1), phosphoryl-mixed lineage kinase domain-like protein (p-MLKL) and caspase-3. This downregulation of necroptosis and apoptosis ultimately led to a reduction of inflammatory factors and damage-associated molecular patterns (DAMPs), such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL- 1β), and interleukin-6 (IL-6) and high mobility group protein B1(HMGB1) in the lungs, thereby ameliorating COPD.
conclusionsOur findings suggest that miR-21 contributes to the worsening of chronic obstructive pulmonary disease by modulating necroptosis and apoptosis in bronchial epithelial cells, providing a new theoretical basis for the pathogenesis of chronic obstructive pulmonary disease.
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