CAJ | 학술논문

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 re-ceptors，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。
세포정서성배사（ necroptosis）시일충신형적세포사망방식。목전연구적최다적궤제위사망수체（ death re-ceptors，DRs）개도적신호전도도경。수체교호작용단백（receptor interaction protein ，RIP）1화3시necroptosis신호통로중겁위중요적조절단백。병차necroptosis능유도상관적염증반응，가중조직손상。신근연구표명뇌결혈후뇌조직적손상여necroptosis밀절상관。본문취necroptosis적궤제급유관신경보호방면적분자파향연구진전진행종술。
Necroptosis is a new type of cell death.Up to now the best investigated mechanism is death receptors-in-duced 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 mech-anisms of necroptosis and the molecular targets of neural protection.