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.
引用
收藏
页码:3989 / 3998
页数:9
相关论文
共 871 条
[1]  
Chouchani ET(2016)A unifying mechanism for mitochondrial superoxide production during ischemia–reperfusion injury Cell Metab 23 254-263
[2]  
Pell VR(2015)Melatonin prevents cell death and mitochondrial dysfunction via a SIRT1-dependent mechanism during ischemic-stroke in mice J Pineal Res 58 61-70
[3]  
James AM(2016)Expanding the concept of neuroprotection for acute ischemic stroke: the pivotal roles of reperfusion and the collateral circulation Prog Neurobiol 145–146 46-77
[4]  
Work LM(2009)Melatonin protects against heart ischemia–reperfusion injury by inhibiting mitochondrial permeability transition pore opening Am J Physiol Heart Circ Physiol 297 H1487-H1493
[5]  
Saeb-Parsy K(2017)Defective branched-chain amino acid catabolism disrupts glucose metabolism and sensitizes the heart to ischemia–reperfusion injury Cell Metab 25 374-385
[6]  
Frezza C(2003)Protective effect of melatonin against mitochondrial injury induced by ischemia and reperfusion of rat liver Eur J Pharmacol 469 145-152
[7]  
Krieg T(2015)Fatty acid binding protein-4 (FABP4) is a hypoxia inducible gene that sensitizes mice to liver ischemia/reperfusion injury J Hepatol 63 855-862
[8]  
Murphy MP(2013)Melatonin treatment improves adipose-derived mesenchymal stem cell therapy for acute lung ischemia–reperfusion injury J Pineal Res 54 207-221
[9]  
Yang Y(2015)Combined melatonin and exendin-4 therapy preserves renal ultrastructural integrity after ischemia–reperfusion injury in the male rat J Pineal Res 59 434-447
[10]  
Jiang S(2012)Crucial role of SLP-76 and ADAP for neutrophil recruitment in mouse kidney ischemia–reperfusion injury J Exp Med 209 407-421