Background: Cigarette smoking-induced oxidant-antioxidant imbalance is a factor that contributes to the pathogenesis of COPD through epithelial cell apoptosis. Irisin is a skeletal muscle cell-derived myokine associated with physical activity. Irisin is also known to decrease oxidant-induced apoptosis in patients with diabetes mellitus. However, the correlation between irisin and emphysema in COPD and its role in epithelial cell apoptosis remains unknown.
Subjects And Methods: Forty patients with COPD were enrolled in this study. Pulmonary function tests and measurements of the percentage of low-attenuation area on high-resolution computed tomography images were performed, and the results were evaluated for correlation with serum irisin levels. The effect of irisin on cigarette-smoke extract-induced A549 cell apoptosis and the expression of Nrf2, a transcription factor for antioxidants, was also examined in vitro.
Results: Serum irisin levels were significantly correlated with lung diffusing capacity for carbon monoxide divided by alveolar volume (=0.56, <0.01) and percentage of low-attenuation area (=-0.79, <0.01). Moreover, irisin significantly enhanced Nrf2 expression (<0.05) and reduced cigarette-smoke extract-induced A549 cell apoptosis (<0.05).
Conclusion: Decreased serum irisin levels are related to emphysema in patients with COPD and involved in epithelial apoptosis, resulting in emphysema. Irisin could be a novel treatment for emphysema in patients with COPD.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5344413 | PMC |
http://dx.doi.org/10.2147/COPD.S126233 | DOI Listing |
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