脑缺血后necroptosis的机制及神经保护

Mechanisms and neuroprotection of necroptosis after cerebral ischemia

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。

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 neeroptosis. 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 nccroptosis and the molecular targets of neural protection.