中文摘要：

细胞死亡一直以来被简单分为凋亡和坏死两种主要形式，其中坏死被公认为是组织细胞受到损害因素下发生的被动、不可逆、非调控性的死亡过程。然而最新的研究证实，在某些特定条件下坏死仍可受到调控并具有被逆转的可能，这种新型细胞死亡方式被称为程序性坏死。程序性坏死途径参与了生物体的生长发育、衰老和死亡等生理学进程，尤其在多种神经系统疾病（颅脑创伤、感染、神经退行性病变）的发生、发展中扮演了重要角色。受体相互作用蛋白-3（RIP3）作为细胞凋亡和坏死之间相互转换的关键性分子，在介导神经细胞损伤的程序性坏死、NF-κB通路激活以及诱发线粒体活性氧自由基（ROS）的生成等机制中发挥着重要作用。本文就RIP3的分子功能及其与神经疾病的关系进展予以综述。

英文摘要：

Cell death has been divided into two main forms, apoptosis and necrosis. Owing to the non-renewable neuron, classic studies showed that necrosis is considered to be passive and irreversible. However, the latest studies showed that cell death of lesions is not completely induced by damage, but by the complex regulation of cellular signaling conduction systems, which belonged to the biology negative feedback regulation of reaction to signal stimulation. Neeroptosis involved in the organism developing, aging and death, especially in the nervous system diseases, such as the occurrence and development of traumatic brain injury （TBI）I infection and neural degenerative diseases. Receptor-interacting protein 3 （RIP3） is a key molecular in mediated programmed cell necrosis （necroptosis） pathway, which plays an important role in mediating the necroptosis necrotizing apoptosis of nerve cell damage, the NF-κB signaling pathway activation and mitochondrial reactive oxygen species （ROS） generation. Here is to make a review of research progress in the RIP3 function and the relationship between RIP3 and neuronal diseases.