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Melatonin and mitochondrial function during ischemia/reperfusion injury

  • Multi-author review
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An Author Correction to this article was published on 24 April 2018

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Abstract

Ischemia/reperfusion (IR) injury occurs in many organs and tissues, and contributes to morbidity and mortality worldwide. Melatonin, an endogenously produced indolamine, provides a strong defense against IR injury. Mitochondrion, an organelle for ATP production and a decider for cell fate, has been validated to be a crucial target for melatonin to exert its protection against IR injury. In this review, we first clarify the mechanisms underlying mitochondrial dysfunction during IR and melatonin’s protection of mitochondria under this condition. Thereafter, special focus is placed on the protective actions of melatonin against IR injury in brain, heart, liver, and others. Finally, we explore several potential future directions of research in this area. Collectively, the information compiled here will serve as a comprehensive reference for the actions of melatonin in IR injury identified to date and will hopefully aid in the design of future research and increase the potential of melatonin as a therapeutic agent.

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Change history

  • 24 April 2018

    In the original publication, affiliations were incorrectly published for the authors.

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Acknowledgements

This work was supported by the National Natural Science Foundation of China (81500263) and China Postdoctoral Science Foundation (2016T90973 and 2015M572681).

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Ma, Z., Xin, Z., Di, W. et al. Melatonin and mitochondrial function during ischemia/reperfusion injury. Cell. Mol. Life Sci. 74, 3989–3998 (2017). https://doi.org/10.1007/s00018-017-2618-6

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