C-Jun N-Terminal Kinases and Their Pharmacological Modulation in Ischemic and Reperfusion Brain Injury; Neuroscience and Behavioral Physiology; Vol. 48, iss. 6
| Parent link: | Neuroscience and Behavioral Physiology.— , 1967- Vol. 48, iss. 6.— 2019.— [P. 721–728] |
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| 企業作者: | |
| 其他作者: | , , , |
| 總結: | Title screen 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. Режим доступа: по договору с организацией-держателем ресурса |
| 語言: | 英语 |
| 出版: |
2019
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| 主題: | |
| 在線閱讀: | https://doi.org/10.1007/s11055-018-0622-4 |
| 格式: | 電子 Book Chapter |
| KOHA link: | https://koha.lib.tpu.ru/cgi-bin/koha/opac-detail.pl?biblionumber=664088 |
| 總結: | Title screen 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. Режим доступа: по договору с организацией-держателем ресурса |
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| DOI: | 10.1007/s11055-018-0622-4 |