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缺血/再灌注损伤期间的褪黑素与线粒体功能

Melatonin and mitochondrial function during ischemia/reperfusion injury.

作者信息

Ma Zhiqiang, Xin Zhenlong, Di Wencheng, Yan Xiaolong, Li Xiaofei, Reiter Russel J, Yang Yang

机构信息

Key Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, Faculty of Life Sciences, UT Health San Antonio, 229 Taibai North Road, Xi'an, 710069, China.

Department of Thoracic Surgery, Tangdu Hospital, Fourth Military Medical University, 1 Xinsi Road, Xi'an, 710038, China.

出版信息

Cell Mol Life Sci. 2017 Nov;74(21):3989-3998. doi: 10.1007/s00018-017-2618-6. Epub 2017 Aug 9.

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.

摘要

缺血/再灌注(IR)损伤发生于许多器官和组织,是全球范围内发病和死亡的原因之一。褪黑素是一种内源性产生的吲哚胺,对IR损伤具有强大的防御作用。线粒体是产生ATP的细胞器,也是细胞命运的决定者,已被证实是褪黑素发挥其抗IR损伤保护作用的关键靶点。在本综述中,我们首先阐明IR期间线粒体功能障碍的潜在机制以及在此条件下褪黑素对线粒体的保护作用。此后,重点关注褪黑素对脑、心脏、肝脏等器官IR损伤的保护作用。最后,我们探索该领域未来几个潜在的研究方向。总体而言,此处汇编的信息将作为迄今为止已确定的褪黑素在IR损伤中的作用的全面参考资料,并有望有助于未来研究的设计,提高褪黑素作为治疗剂的潜力。

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Melatonin and mitochondrial function during ischemia/reperfusion injury.缺血/再灌注损伤期间的褪黑素与线粒体功能
Cell Mol Life Sci. 2017 Nov;74(21):3989-3998. doi: 10.1007/s00018-017-2618-6. Epub 2017 Aug 9.

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