| 摘要: |
| [摘要] 细胞程序性坏死（necroptosis）是一种新型的细胞死亡方式。目前研究的最多的机制为死亡受体（death receptors，DRs）介导的信号转导途径。受体交互作用蛋白（receptor interaction protein ，RIP）1和3是necroptosis信号通路中极为重要的调节蛋白。并且necroptosis能诱导相关的炎症反应，加重组织损伤。新近研究表明脑缺血后脑组织的损伤与necroptosis密切相关。本文就necroptosis的机制及有关神经保护方面的分子靶向研究进展进行综述。 |
| 关键词: 脑缺血 necroptosis 受体交互作用蛋白 炎症反应 |
| DOI：10.11724/jdmu.2015.02.22 |
| 分类号: |
| 基金项目: |
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| Mechanisms and neuroprotection of necroptosis after cerebral ischemia |
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DENG Xi-jia 1,WANG Peng-xu 1,TONG Tong 1,LIN Jing 1,JIANG Chun-ling 21,2
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1.Seven-year Graduate Program 2010;2.Department of Physiology,Dalian Medical University,Dalian 116044,China
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| Abstract: |
| [Abstract] Necroptosis is a new type of cell death. Up to now the best investigated mechanism is death receptors-induced signaling pathway. Receptor interaction protein 1 (RIP1) and 3 (RIP3) play crucial roles in the signaling pathway of necroptosis. In addition,necroptosis can induce inflammation and increase tissue damage. Recent studies have shown that brain tissue damage is closely related to necroptosis after cerebral ischemia. In this article,we have reviewed the mechanisms of necroptosis and the molecular targets of neural protection. |
| Key words: [Key words] cerebral ischemia necroptosis RIP inflammation |
