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RIP3 in Necroptosis: Underlying Contributions to Traumatic Brain Injury

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Abstract

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.

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This work was supported by the Natural Science Foundation of Zhejiang Province (no. LY19H170001).

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Xuehong Liu designed the study. Lvxia Wang, Yong Zhang, Min Huang and Xuehong Liu prepared the first draft of the manuscript. Lvxia Wang, Yong Zhang, Min Huang and Xuehong Liu revised the manuscript. All authors approved the final paper.

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Wang, L., Zhang, Y., Huang, M. et al. RIP3 in Necroptosis: Underlying Contributions to Traumatic Brain Injury. Neurochem Res 49, 245–257 (2024). https://doi.org/10.1007/s11064-023-04038-z

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