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Melatonin and mitochondrial function during ischemia/reperfusion injury
- Ma, Zhiqiang, Xin, Zhenlong, Di, Wencheng, Yan, Xiaolong, Li, Xiaofei, Reiter, RusselJ., Yang, Yang
- Cellular and molecular life sciences 2017 v.74 no.21 pp. 3989-3998
- adenosine triphosphate, brain, heart, ischemia, liver, melatonin, mitochondria, morbidity, mortality, tissues
- 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.