ArticleInternational journal of biological sciences2022
Regulation of lung epithelial cell senescence in smoking-induced COPD/emphysema by microR-125a-5p via Sp1 mediation of SIRT1/HIF-1a.
Article in International journal of biological sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.
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Who cites it
58 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.
- MicroRNAs and Cellular Senescence in Melanoma: An Underexplored Link to Tumor Progression-A Systematic Review with Bioinformatics Analyses.International journal of molecular sciences · 2026Pooled it
- MiR-342-3p Attenuates Inflammation and Pyroptosis in Severe Community-Acquired Pneumonia by Targeting EP300.Biochemical genetics · 2026Article
- Conserved signaling pathways and transcriptional regulators drive ovarian aging across species.Poultry science · 2026Article
- Extracellular vesicles in senescence-associated chronic lung diseases.Chinese medical journal · 2026Review
- Integrating network pharmacology, molecular docking, machine learning, and experimental validation: puerarin improves sepsis-induced acute kidney injury via the Sirt1-Nrf2-HO-1 pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Review
- Emerging role of SIRT1 in asthma and COPD from molecular mechanisms to translational therapy.iScience · 2026Review
- Article
- miR-495-3p promotes chronic obstructive pulmonary disease by activating ferroptosis in lung epithelial cells through regulation of the ETS1/GPX4 axis.Molecular biology reports · 2026Article
- Integrative Approaches to Treating Cellular Senescence in Kidney Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Bronchial epithelial-derived exosomal SLC6A14 promotes airway inflammation and mucus hypersecretion via the ZFP36L1/IL-8 axis.Functional & integrative genomics · 2026Article
- SP1 recruits TET1 to mediate Kif1a demethylation and synaptic remodeling in a mouse model of chronic migraine.The journal of headache and pain · 2026Article
- Article
- Spatial and single-cell transcriptomics reveal a HIF-1α/NF-κB-driven hypoxia-induced senescence axis in BPH epithelium.International journal of biological sciences · 2026Article
- Hypoxia: a critical pathophysiological driver in respiratory inflammatory diseases.Military Medical Research · 2026Review
- β2-Microglobulin Induces Mitochondrial Dysfunction Accompanied by Bronchial Epithelial Cell Senescence.International journal of chronic obstructive pulmonary disease · 2026Article
- Sulforaphane attenuates oxidative stress, senescence, and ferroptosis induced by cigarette smoke extractResearch in pharmaceutical sciences · 2025Article
- Aging and lung diseases: Unraveling mechanisms and therapeutic targets.Chinese medical journal pulmonary and critical care medicine · 2025Review
- Investigation of expression levels of MIR125A and MIR126 genes in chronic obstructive lung disease.Molecular biology reports · 2025Article
- Histone H4 Lysine 12 Lactylation Promotes the Senescence of Alveolar Epithelial Type II Cells in Chronic Obstructive Pulmonary Disease by Modulating the CD38-NADAging and disease · 2025Article
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic obstructive pulmonary disease (COPD) affects the health of more than 300 million people worldwide; at present, there is no effective drug to treat COPD. Smoking is the most important risk factor, but the molecular mechanism by which smoking causes the disease is unclear. The senescence of lung epithelial cells is related to development of COPD. Regulation of miRNAs is the main epigenetic mechanism related to aging. β-Galactose staining showed that the lung tissues of smokers have a higher degree of cellular senescence, and the expression of miR-125a-5p is high. This effect is obvious for smokers with COPD/emphysema, and there is a negative correlation between miR-125a-5p levels and values for forced expiratory volume in one second (FEV1)/forced vital capacity (FVC). After Balb/c mice were chronically exposed to various concentrations of cigarette smoke (CS), plethysmography showed that lung function was impaired, lung tissue senescence was increased, and the senescence-associated secretory phenotype (SASP) in bronchoalveolar lavage fluid was increased. For mouse lung epithelial (MLE)-12 cells treated with cigarette smoke extract (CSE), Sp1 and SIRT1 levels were low, HIF-1α acetylation levels were high, and cell senescence and secretion of SASP factors were elevated. Down-regulation of miR-125a-5p or up-regulation of Sp1 reversed these effects. In addition, compared with mice exposed to CS, knockdown of miR-125a-5p reduced lung epithelial cell senescence and COPD/emphysema. Therefore, in smoking-induced COPD, elevated miR-125a-5p participates in the senescence of lung epithelial cells through Sp1/SIRT1/HIF-1α. These findings provide evidence related to the pathogenesis of COPD/emphysema caused by chronic smoking.
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