Melatonin and mitochondrial function during ischemia/reperfusion injury

被引:0
作者
Zhiqiang Ma
Zhenlong Xin
Wencheng Di
Xiaolong Yan
Xiaofei Li
Russel J. Reiter
Yang Yang
机构
[1] UT Health San Antonio,Key Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Faculty of Life Sciences
[2] Fourth Military Medical University,Department of Thoracic Surgery, Tangdu Hospital
[3] Fourth Military Medical University,Department of Biomedical Engineering
[4] Nanjing University Medical School,Department of Cardiology, Affiliated Drum Tower Hospital
[5] UT Health Science Center,Department of Cellular and Structural Biology
来源
Cellular and Molecular Life Sciences | 2017年 / 74卷
关键词
Melatonin; Mitochondria; Ischemia/reperfusion injury; Oxidative stress;
D O I
暂无
中图分类号
学科分类号
摘要
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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页码:3989 / 3998
页数:9
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