Open Access

AMPK activation serves a critical role in mitochondria quality control via modulating mitophagy in the heart under chronic hypoxia

  • Authors:
    • Huagang Zhang
    • Bo Liu
    • Tianbo Li
    • Yun Zhu
    • Guiping Luo
    • Yunhan Jiang
    • Fuqin Tang
    • Zhao Jian
    • Yingbin Xiao
  • View Affiliations

  • Published online on: October 26, 2017     https://doi.org/10.3892/ijmm.2017.3213
  • Pages:69-76
  • Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Mitochondrial biogenesis is one of the generally accepted regulatory mechanisms in the heart under chronic hypoxia. The precise quantity and quality control of mitochondria is critical for the survival and function of cardiomyocytes. Mitochondrial autophagy, also known as mitophagy, which selectively eliminates dysfunctional and unwanted mitochondria, is the most important type of mitochondrial quality control. However, the detailed molecular mechanisms of mitophagy in cardiomyocytes have been largely undefined. The present study investigated the role of adenosine 5'‑monophosphate‑activated protein kinase (AMPK) in mitophagy regulation in cardiomyocytes under chronic hypoxia. H9c2 cells were cultured under hypoxic conditions (1% O2) for different time periods. Mitochondrial biogenesis was confirmed and hypoxia was found to induce the collapse of mitochondrial membrane potential (ΛΨm) and increase the number of dysfunctional mitochondria. As expected, mitochondrial autophagy was increased significantly in cardiomyocytes exposed to hypoxic conditions for 48 h. AMPK was activated under hypoxia. Notably, when the activation of AMPK was enhanced by the AMPK agonist AICAR, mitochondrial autophagy was increased accordingly. By contrast, when AMPK activation was blocked, mitochondrial autophagy was decreased and cardiomyocyte apoptosis was increased. In conclusion, in the present study, mitophagy was activated and played a crucial role in cardioprotection under chronic hypoxia. AMPK was involved in mitophagy regulation, thereby providing a potential therapeutic target for heart diseases associated with chronic hypoxia.

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January 2018
Volume 41 Issue 1

Print ISSN: 1107-3756
Online ISSN:1791-244X

2016 Impact Factor: 2.341
Ranked #21/128 Medicine Research and Experimental
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APA
Zhang, H., Liu, B., Li, T., Zhu, Y., Luo, G., Jiang, Y. ... Xiao, Y. (2018). AMPK activation serves a critical role in mitochondria quality control via modulating mitophagy in the heart under chronic hypoxia. International Journal of Molecular Medicine, 41, 69-76. https://doi.org/10.3892/ijmm.2017.3213
MLA
Zhang, H., Liu, B., Li, T., Zhu, Y., Luo, G., Jiang, Y., Tang, F., Jian, Z., Xiao, Y."AMPK activation serves a critical role in mitochondria quality control via modulating mitophagy in the heart under chronic hypoxia". International Journal of Molecular Medicine 41.1 (2018): 69-76.
Chicago
Zhang, H., Liu, B., Li, T., Zhu, Y., Luo, G., Jiang, Y., Tang, F., Jian, Z., Xiao, Y."AMPK activation serves a critical role in mitochondria quality control via modulating mitophagy in the heart under chronic hypoxia". International Journal of Molecular Medicine 41, no. 1 (2018): 69-76. https://doi.org/10.3892/ijmm.2017.3213