ArticleBMC pulmonary medicine2024
Lung transcriptomics reveals the underlying mechanism by which aerobic training enhances pulmonary function in chronic obstructive pulmonary disease.
Article in BMC pulmonary medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 2 citations in OpenAlex.
- Wnt/Chemerin Signaling Involved in Exercise Training Preventing Diaphragm Dysfunction Induced by Cigarette Smoke.Biomedicines · 2026Article
- Multi-Omics Analysis Reveals New Insights into Yak Lung Under High-Altitude Adaptation.Animals : an open access journal from MDPI · 2026Article
- Sexually distinct multi-omic responses to progressive endurance exercise training in the rat lung.American journal of respiratory cell and molecular biology · 2026Article
- An Animal Model of Liuzijue Based on Kinematic Features Exploration: A Pilot Study Conducting in COPD.Immunity, inflammation and disease · 2025Article
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundAerobic training is the primary method of rehabilitation for improving respiratory function in patients with chronic obstructive pulmonary disease (COPD) in remission. However, the mechanism underlying this improvement is not yet fully understood. The use of transcriptomics in rehabilitation medicine offers a promising strategy for uncovering the ways in which exercise training improves respiratory dysfunction in COPD patients. In this study, lung tissue was analyzed using transcriptomics to investigate the relationship between exercise and lung changes.
methodsMice were exposed to cigarette smoke for 24 weeks, followed by nine weeks of moderate-intensity treadmill exercise, with a control group for comparison. Pulmonary function and structure were assessed at the end of the intervention and RNA sequencing was performed on the lung tissue.
resultsExercise training was found to improve airway resistance and lung ventilation indices in individuals exposed to cigarette smoke. However, the effect of this treatment on damaged alveoli was weak. The pair-to-pair comparison revealed numerous differentially expressed genes, that were closely linked to inflammation and metabolism.
conclusionsFurther research is necessary to confirm the cause-and-effect relationship between the identified biomarkers and the improvement in pulmonary function, as this was not examined in the present study.
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