炎症和细胞死亡过程积极地控制机体器官的稳态。受体相互作用蛋白激酶1 (RIPK1) 是RIPK家族的成员，是细胞死亡和炎症的关键调节因子，并在细胞和组织层面调控稳态。程序性坏死相关的坏死（necroptosis）和肿瘤坏死因子（TNF）诱导的坏死性细胞死亡主要由RIPK1的激酶活性调控。因此，RIPK1最近成为一个上游激酶，控制多条细胞途径并参与调节炎症和细胞死亡。中枢神经系统（CNS）中的所有主要细胞类型均表达RIPK1。选择性抑制RIPK1已被证明可以预防神经元细胞死亡，从而可能显著减少神经退行性疾病和神经炎症。此外，RIPK1的激酶结构非常有利于开发特异性药物小分子抑制剂。这些因素导致RIPK1成为阿尔茨海默病的重要治疗靶点。 版权所有 © 2023 Elsevier Ltd. 保留所有权利。

Inflammation and cell death processes positively control the organ homeostasis of an organism. Receptor-interacting protein kinase 1 (RIPK1), a member of the RIPK family, is a crucial regulator of cell death and inflammation, and control homeostasis at the cellular and tissue level. Necroptosis, a programmed form of necrosis-mediated cell death and tumor necrosis factor (TNF)-induced necrotic cell death, is mostly regulated by RIPK1 kinase activity. Thus, RIPK1 has recently emerged as an upstream kinase that controls multiple cellular pathways and participates in regulating inflammation and cell death. All the major cell types in the central nervous system (CNS) have been found to express RIPK1. Selective inhibition of RIPK1 has been shown to prevent neuronal cell death, which could ultimately lead to a significant reduction of neurodegeneration and neuroinflammation. In addition, the kinase structure of RIPK1 is highly conducive to the development of specific pharmacological small-molecule inhibitors. These factors have led to the emergence of RIPK1 as an important therapeutic target for Alzheimer's disease (AD).Copyright © 2023 Elsevier Ltd. All rights reserved.