Exercise training and muscle–lung crosstalk: The emerging roles of Irisin and Semaphorin-3A in pulmonary diseases. A narrative review

Document Type : Review Articles

Authors

1 Chemical Injuries Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran.

2 Exercise Physiology Research Center, Life Style Institute, Baqiyatallah University of Medical Sciences, Tehran, Iran

3 Department of Physical Education and Sport Sciences, West Tehran Branch, Islamic Azad University, Tehran, Iran

Abstract

COPD is an inflammatory disorder caused by prolonged inhalation of harmful substances such as cigarette smoke that leads to an irreversible respiratory disorder. Airway obstruction usually has a progressive period characterized by chronic cough, sputum production, and dyspnea, resulting in decreased physical activity. Two hypotheses have been proposed for the pathogenesis of lung diseases, especially COPD, including the oxidant-antioxidant imbalance hypothesis and the protease-antioxidant imbalance hypothesis. Oxidants can cause irreversible damage to lung cells. Oxidants activate inflammatory gene expression primarily through NFκB signaling. Increase inflammation promotes apoptosis in the epithelial cells, endothelial cells, and airways, that resulting Emphysema. This pathological period causes progress the disease. Recently, has been shown that decreased physical activity is associated with COPD injuries, and the level of physical activity is most associated with COPD mortality. Therefore, the tendency to maintain and improve the physical activity of pulmonary patients, especially COPD was increased. In lung diseases, muscle mass usually decreases and severe atrophy occurs. Most studies suggest increased mobility and exercise to enhance cardiorespiratory endurance and decrease atrophy. However, the exact biological mechanism for the recovery of patients with COPD after a physical activity has not been explained. Exercise can produce Irisin and Semaphorin-3A by stimulating muscle and nerve cell, which have positive effects on other tissues, including the lungs. Limited studies have examined the role of these factors in lung tissue. Therefore, in this mini-review, the lung muscle cross-talk is examined by evaluating the role of Irisin and Semaphorin-3A.

What is already known on this subject?

Previous studies have only examined the positive effects of increasing serum levels of Irisin on the lung parenchyma and reducing COPD-induced emphysema.

 

What this study adds?

The present study showed that in addition to Irisin, semaphorin-3A induced by muscle contraction, prevents inflammation and lung damage caused by COPD or other lung disease.

Keywords

Main Subjects

References

Boström, P., Wu, J., Jedrychowski, M. P., Korde, A., Ye, L., Lo, J. C., . . . Long, J. Z. (2012). A PGC1-α-dependent myokine that drives brown-fat-like development of white fat and thermogenesis. Nature, 481(7382), 463-468. doi: https://doi.org/10.1038/nature10777
Buscemi, S., Corleo, D., Vasto, S., Buscemi, C., Barile, A. M., Rosafio, G. Galvano, F. (2020). Serum irisin concentrations in severely inflamed patients. Hormone and Metabolic Research, 52(04), 246-250. doi: 10.1055/a-1111-9249
Hogg, J. C., & Timens, W. (2009). The pathology of chronic obstructive pulmonary disease. Annual Review of Pathology: Mechanisms of Disease, 4, 435-459. doi: https://doi.org/10.1146/annurev.pathol.4.110807.092145
Hou, G., Yin, Y., Han, D., Wang, Q.-y., & Kang, J. (2015). Rosiglitazone attenuates the metalloprotease/anti-metalloprotease imbalance in emphysema induced by cigarette smoke: involvement of extracellular signal-regulated kinase and NFκB signaling. International journal of chronic obstructive pulmonary disease, 10, 715. doi: 10.2147/COPD.S77514
Ijiri, N., Kanazawa, H., Asai, K., Watanabe, T., & Hirata, K. (2015). Irisin, a newly discovered myokine, is a novel biomarker associated with physical activity in patients with chronic obstructive pulmonary disease. Respirology, 20(4), 612-617. doi: https://doi.org/10.1111/resp.12513
Kensler, T. W., Wakabayashi, N., & Biswal, S. (2007). Cell survival responses to environmental stresses via the Keap1-Nrf2-ARE pathway. Annu. Rev. Pharmacol. Toxicol., 47, 89-116. doi: https://doi.org/10.1146/annurev.pharmtox.46.120604.141046
Liu, S. W., Qiao, S. B., Yuan, J. S., & Liu, D. Q. (2009). Association of plasma visfatin levels with inflammation, atherosclerosis and acute coronary syndromes (ACS) in humans. Clinical endocrinology, 71(2), 202-207. doi: https://doi.org/10.1111/j.1365-2265.2008.03453.x
Luk, T., Malam, Z., & Marshall, J. C. (2008). Pre‐B cell colony‐enhancing factor (PBEF)/visfatin: a novel mediator of innate immunity. Journal of leukocyte biology, 83(4), 804-816. doi: https://doi.org/10.1189/jlb.0807581
MacNee, W., Rabinovich, R. A., & Choudhury, G. (2014). Ageing and the border between health and disease. European Respiratory Journal, 44(5), 1332-1352. doi: 10.1183/09031936.00134014
Moschen, A. R., Kaser, A., Enrich, B., Mosheimer, B., Theurl, M., Niederegger, H., & Tilg, H. (2007). Visfatin, an adipocytokine with proinflammatory and immunomodulating properties. The Journal of Immunology, 178(3), 1748-1758. doi: https://doi.org/10.4049/jimmunol.178.3.1748
Rangasamy, T., Misra, V., Zhen, L., Tankersley, C. G., Tuder, R. M., & Biswal, S. (2009). Cigarette smoke-induced emphysema in A/J mice is associated with pulmonary oxidative stress, apoptosis of lung cells, and global alterations in gene expression. American Journal of Physiology-Lung Cellular and Molecular Physiology, 296(6), L888-L900. doi: https://doi.org/10.1152/ajplung.90369.2008
Segura-Valdez, L., Pardo, A., Gaxiola, M., Uhal, B. D., Becerril, C., & Selman, M. (2000). Upregulation of gelatinases A and B, collagenases 1 and 2, and increased parenchymal cell death in COPD. Chest, 117(3), 684-694. doi: https://doi.org/10.1378/chest.117.3.684
Song, H., Wu, F., Zhang, Y., Zhang, Y., Wang, F., Jiang, M., . . . Yang, L. (2014). Irisin promotes human umbilical vein endothelial cell proliferation
through the ERK signaling pathway and partly suppresses high glucose-induced apoptosis. PLoS ONE, 9(10), e110273. doi: https://doi.org/10.1371/journal.pone.0110273
Sugiyama, Y., Asai, K., Yamada, K., Kureya, Y., Ijiri, N., Watanabe, T., . . . Hirata, K. (2017). Decreased levels of irisin, a skeletal muscle cell-derived myokine, are related to emphysema associated with chronic obstructive pulmonary disease. International journal of chronic obstructive pulmonary disease, 12, 765. doi:
Tatsumi, R., Sankoda, Y., Anderson, J. E., Sato, Y., Mizunoya, W., Shimizu, N., . . . Ikeuchi, Y. (2009). Possible implication of satellite cells in regenerative motoneuritogenesis: HGF upregulates neural chemorepellent Sema3A during myogenic differentiation. American Journal of Physiology-Cell Physiology, 297(2), C238-C252. doi: 10.2147/COPD.S126233
Vestbo, J., Hurd, S. S., Agustí, A. G., Jones, P. W., Vogelmeier, C., Anzueto, A., . . . Nishimura, M. (2013). Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: GOLD executive summary. American journal of respiratory and critical care medicine, 187(4), 347-365. doi: https://doi.org/10.1152/ajpcell.00161.2009
Wu, F., Song, H., Zhang, Y., Zhang, Y., Mu, Q., Jiang, M., . . . Li, H. (2015). Irisin induces angiogenesis in human umbilical vein endothelial cells in vitro and in zebrafish embryos in vivo via activation of the ERK signaling pathway. PLoS ONE, 10(8), e0134662. doi: https://doi.org/10.1371/journal.pone.0134662
Yamada, K., Asai, K., Nagayasu, F., Sato, K., Ijiri, N., Yoshii, N., . . . Kanazawa, H. (2016). Impaired nuclear factor erythroid 2-related factor 2 expression increases apoptosis of airway epithelial cells in patients with chronic obstructive pulmonary disease due to cigarette smoking. BMC pulmonary medicine, 16(1), 1-10.  doi: https://doi.org/10.1186/s12890-016-0189-1
Zhu, D., Wang, H., Zhang, J., Zhang, X., Xin, C., Zhang, F., . . . Yan, W. (2015). Irisin improves endothelial function in type 2 diabetes through reducing oxidative/nitrative stresses. Journal of molecular and cellular cardiology, 87, 138-147. doi: https://doi.org/10.1016/j.yjmcc.2015.07.015
Journal of Exercise & Organ Cross Talk
Volume 1, Issue 1
June 2021
Pages 24-28

Files

History

  • Receive Date: 10 April 2021
  • Revise Date: 10 June 2021
  • Accept Date: 13 June 2021

Share

How to cite

Statistics