c-Jun N-Terminal Kinases and Their Pharmacological Modulation in Ischemic and Reperfusion Brain Injury

被引：0
作者：
Shvedova M.V. [1 ,5 ]
Anfinogenova Y.D. [1 ,2 ,5 ]
Shchepetkin I.A. [1 ,4 ]
Atochin D.N. [1 ,3 ]
机构：
[1] Tomsk RASA Center, Tomsk Polytechnic University, Tomsk
[2] Research Institute of Cardiology, Tomsk National Medical Research Center, Tomsk
[3] Cardiovascular Research Center and Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA
[4] Department of Microbiology and Immunology, Montana State University, Bozeman, MT
[5] Siberian State Medical University, Tomsk
来源：
Neuroscience and Behavioral Physiology | 2018年 / 48卷 / 6期
关键词：
brain; c-Jun N-terminal kinase; ischemic-reperfusion injury; JNK inhibitor; stroke; therapeutic target;
D O I：
10.1007/s11055-018-0622-4
中图分类号：
学科分类号：
摘要：
We present here a review of the literature on the role of c-Jun N-terminal kinases (JNK) and their inhibitors in ischemic and reperfusion brain injuries. The functions of JNK in the signal mechanisms involved in brain damage in ischemia and reperfusion are discussed. Effects linked with inhibition of JNK with synthetic and natural compounds in experimental models of ischemia and reperfusion brain injury are described. Results from experimental studies show that JNK provide potential therapeutic targets for protecting the brain from ischemic stroke. However, the fact that JNK have numerous physiological functions prevents systematic use of nonspecific inhibitors of these kinases for therapeutic purposes. The authors conclude that this task requires a further search for selective JNK3 inhibitors. © 2018, Springer Science+Business Media, LLC, part of Springer Nature.
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页码：721 / 728
页数：7
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