Open Access

Swimming exercise inhibits myocardial ER stress in the hearts of aged mice by enhancing cGMP‑PKG signaling

  • Authors:
    • Pan Chang
    • Xiaomeng Zhang
    • Mingyang Zhang
    • Guohua Li
    • Lang Hu
    • Huishou Zhao
    • Xiaoxing Zhu
    • Juan Wu
    • Xihui Wang
    • Kaiyan Wang
    • Jing Zhang
    • Minggang Ren
    • Baoying Chen
    • Xiaoling Zhu
    • Miaozhang Zhu
    • Jun Yu
  • View Affiliations

  • Published online on: December 5, 2019     https://doi.org/10.3892/mmr.2019.10864
  • Pages: 549-556
  • Copyright: © Chang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The purpose of the present study was to explore aging‑associated cardiac dysfunction and the possible mechanism by which swimming exercise modulates cardiac dysfunction in aged mice. Aged mice were divided into two groups: i) Aged mice; and ii) aged mice subjected to swimming exercises. Another cohort of 4‑month‑old male mice served as the control group. Cardiac structure and function in mice were analyzed using hematoxylin and eosin staining, and echocardiography. The levels of oxidative stress were determined by measuring the levels of superoxide dismutase, malondialdehyde and reactive oxygen species (ROS). Levels of the endoplasmic reticulum (ER) stress‑related protein PKR‑like ER kinase, glucose‑regulated protein 78 and C/EBP homologous protein were determined to evaluate the level of ER stress. The aged group exhibited an abnormal cardiac structure and decreased cardiac function, both of which were ameliorated by swimming exercise. The hearts of the aged mice exhibited pronounced oxidative and ER stress, which were ameliorated by exercise, and was accompanied by the reactivation of myocardial cGMP and suppression of cGMP‑specific phosphodiesterase type 5 (PDE5). The inhibition of PDE5 attenuated age‑induced cardiac dysfunction, blocked ROS production and suppressed ER stress. An ER stress inducer abolished the beneficial effects of the swimming exercise on cardiac function and increased ROS production. The present study suggested that exercise restored cardiac function in mice with age‑induced cardiac dysfunction by inhibiting oxidative stress and ER stress, and increasing cGMP‑protein kinase G signaling.
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February 2020
Volume 21 Issue 2

Print ISSN: 1791-2997
Online ISSN:1791-3004

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APA
Chang, P., Zhang, X., Zhang, M., Li, G., Hu, L., Zhao, H. ... Yu, J. (2020). Swimming exercise inhibits myocardial ER stress in the hearts of aged mice by enhancing cGMP‑PKG signaling. Molecular Medicine Reports, 21, 549-556. https://doi.org/10.3892/mmr.2019.10864
MLA
Chang, P., Zhang, X., Zhang, M., Li, G., Hu, L., Zhao, H., Zhu, X., Wu, J., Wang, X., Wang, K., Zhang, J., Ren, M., Chen, B., Zhu, X., Zhu, M., Yu, J."Swimming exercise inhibits myocardial ER stress in the hearts of aged mice by enhancing cGMP‑PKG signaling". Molecular Medicine Reports 21.2 (2020): 549-556.
Chicago
Chang, P., Zhang, X., Zhang, M., Li, G., Hu, L., Zhao, H., Zhu, X., Wu, J., Wang, X., Wang, K., Zhang, J., Ren, M., Chen, B., Zhu, X., Zhu, M., Yu, J."Swimming exercise inhibits myocardial ER stress in the hearts of aged mice by enhancing cGMP‑PKG signaling". Molecular Medicine Reports 21, no. 2 (2020): 549-556. https://doi.org/10.3892/mmr.2019.10864