文献类型：期刊文献

英文题名：RIP3 in Necroptosis: Underlying Contributions to Traumatic Brain Injury

作者：Wang, Lvxia[1,2];Zhang, Yong[2];Huang, Min[2];Yuan, Yiling[3];Liu, Xuehong[1,2]

机构：[1]Shaoxing Univ, Sch Life Sci, Shaoxing, Zhejiang, Peoples R China;[2]Shaoxing Univ, Sch Med, Dept Histol & Embryol, Shaoxing, Zhejiang, Peoples R China;[3]Univ Durham, Dept Biosci, Durham, England

年份：2023

外文期刊名：NEUROCHEMICAL RESEARCH

收录：SCI-EXPANDED(收录号：WOS:001069072800001)、、WOS

基金：Not applicable.

语种：英文

外文关键词：Receptor-interacting protein kinase 3; Necroptosis; Traumatic brain injury; Receptor-interacting protein kinase 1; Mixed-lineage kinase domain like

外文摘要：Traumatic brain injury (TBI) is a global public safety issue that poses a threat to death, characterized by high fatality rates, severe injuries and low recovery rates. There is growing evidence that necroptosis regulates the pathophysiological processes of a variety of diseases, particularly those affecting the central nervous system. Thus, moderate necroptosis inhibition may be helpful in the management of TBI. Receptor-interacting protein kinase (RIP) 3 is a key mediator in the necroptosis, and its absence helps restore the microenvironment at the injured site and improve cognitive impairment after TBI. In this report, we review different domains of RIP3, multiple analyses of necroptosis, and associations between necroptosis and TBI, RIP3, RIP1, and mixed lineage kinase domain-like. Next, we elucidate the potential involvement of RIP3 in TBI and highlight how RIP3 deficiency enhances neuronal function.