RIP3 in Necroptosis: Underlying Contributions to Traumatic Brain Injury

Overview

Journal Neurochem Res

Specialties Chemistry
Neurology

Date 2023 Sep 24

PMID 37743445

Authors

Lvxia Wang

Yong Zhang

Min Huang

Yiling Yuan

Xuehong Liu

Affiliations

Soon will be listed here.

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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