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Article Open Access

Enalapril attenuates endoplasmic reticulum stress and mitochondrial injury induced by myocardial infarction via activation of the TAK1/NFAT pathway in mice

  • Authors:
    • Xing Rong
    • Donghui Ge
    • Lili Yu
    • Lei Li
    • Maoping Chu
    • Haitao Lv
  • View Affiliations / Copyright

    Affiliations: Department of Cardiology, Children's Hospital of Soochow University, Suzhou, Jiangsu 215025, P.R. China, Children's Heart Center, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Institute of Cardiovascular Development and Translational Medicine, Wenzhou Medical University, Wenzhou, Zhejiang 325027, P.R. China
    Copyright: © Rong et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 972-980
    |
    Published online on: December 4, 2019
       https://doi.org/10.3892/etm.2019.8280
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Abstract

The present study investigated the effect of enalapril on myocardial infarction (MI) and its mechanism of action in mice. Treatment with enalapril significantly attenuated cellular apoptosis and death. In vivo, enalapril treatment alleviated MI injury, and decreased myocardial apoptosis and the size of the infarct area. This was paralleled by increased Bcl‑2 expression, decreased Bax expression, a decreased caspase‑3 level, decreased expression of endoplasmic reticulum stress‑associated proteins, including activating transcription factor 6 and 78 kDa glucose‑regulated protein, and fewer TUNEL‑positive cells in the heart. Furthermore, enalapril‑treatment increased transforming growth factor‑activated kinase 1/nuclear factor of activated T cells 3 signaling, which protected the myocardium.
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Copy and paste a formatted citation
Spandidos Publications style
Rong X, Ge D, Yu L, Li L, Chu M and Lv H: Enalapril attenuates endoplasmic reticulum stress and mitochondrial injury induced by myocardial infarction via activation of the TAK1/NFAT pathway in mice. Exp Ther Med 19: 972-980, 2020.
APA
Rong, X., Ge, D., Yu, L., Li, L., Chu, M., & Lv, H. (2020). Enalapril attenuates endoplasmic reticulum stress and mitochondrial injury induced by myocardial infarction via activation of the TAK1/NFAT pathway in mice. Experimental and Therapeutic Medicine, 19, 972-980. https://doi.org/10.3892/etm.2019.8280
MLA
Rong, X., Ge, D., Yu, L., Li, L., Chu, M., Lv, H."Enalapril attenuates endoplasmic reticulum stress and mitochondrial injury induced by myocardial infarction via activation of the TAK1/NFAT pathway in mice". Experimental and Therapeutic Medicine 19.2 (2020): 972-980.
Chicago
Rong, X., Ge, D., Yu, L., Li, L., Chu, M., Lv, H."Enalapril attenuates endoplasmic reticulum stress and mitochondrial injury induced by myocardial infarction via activation of the TAK1/NFAT pathway in mice". Experimental and Therapeutic Medicine 19, no. 2 (2020): 972-980. https://doi.org/10.3892/etm.2019.8280
Copy and paste a formatted citation
x
Spandidos Publications style
Rong X, Ge D, Yu L, Li L, Chu M and Lv H: Enalapril attenuates endoplasmic reticulum stress and mitochondrial injury induced by myocardial infarction via activation of the TAK1/NFAT pathway in mice. Exp Ther Med 19: 972-980, 2020.
APA
Rong, X., Ge, D., Yu, L., Li, L., Chu, M., & Lv, H. (2020). Enalapril attenuates endoplasmic reticulum stress and mitochondrial injury induced by myocardial infarction via activation of the TAK1/NFAT pathway in mice. Experimental and Therapeutic Medicine, 19, 972-980. https://doi.org/10.3892/etm.2019.8280
MLA
Rong, X., Ge, D., Yu, L., Li, L., Chu, M., Lv, H."Enalapril attenuates endoplasmic reticulum stress and mitochondrial injury induced by myocardial infarction via activation of the TAK1/NFAT pathway in mice". Experimental and Therapeutic Medicine 19.2 (2020): 972-980.
Chicago
Rong, X., Ge, D., Yu, L., Li, L., Chu, M., Lv, H."Enalapril attenuates endoplasmic reticulum stress and mitochondrial injury induced by myocardial infarction via activation of the TAK1/NFAT pathway in mice". Experimental and Therapeutic Medicine 19, no. 2 (2020): 972-980. https://doi.org/10.3892/etm.2019.8280
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