School of Life and Environmental Sciences, Shaoxing University, Zhejiang, China.
Department of Histology and Embryology, School of Medicine, Shaoxing University, Zhejiang, China.
Neurochem Res. 2024 Feb;49(2):245-257. doi: 10.1007/s11064-023-04038-z. Epub 2023 Sep 25.
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.
创伤性脑损伤（TBI）是一个全球性的公共安全问题，对死亡构成威胁，其特点是死亡率高、伤势严重且恢复率低。越来越多的证据表明，坏死性凋亡调节着多种疾病的病理生理过程，特别是那些影响中枢神经系统的疾病。因此，适度抑制坏死性凋亡可能有助于 TBI 的治疗。受体相互作用蛋白激酶（RIP）3 是坏死性凋亡的关键介质，其缺失有助于恢复损伤部位的微环境，并改善 TBI 后的认知障碍。在本报告中，我们回顾了 RIP3 的不同结构域、坏死性凋亡的多种分析以及坏死性凋亡与 TBI、RIP3、RIP1 和混合谱系激酶结构域样蛋白之间的关联。接下来，我们阐明了 RIP3 在 TBI 中的潜在作用，并强调了 RIP3 缺乏如何增强神经元功能。
