RIP3 in Necroptosis: Underlying Contributions to Traumatic Brain Injury.
Neurochem Res
; 49(2): 245-257, 2024 Feb.
Article
em En
| MEDLINE
| ID: mdl-37743445
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.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Apoptose
/
Lesões Encefálicas Traumáticas
Limite:
Humans
Idioma:
En
Revista:
Neurochem Res
Ano de publicação:
2024
Tipo de documento:
Article
País de afiliação:
China