Viral-induced neuronal necroptosis: Detrimental to brain function and regulation by necroptosis inhibitors.
Humans
Protein Kinases
/ metabolism
Inflammasomes
/ metabolism
NLR Family, Pyrin Domain-Containing 3 Protein
/ metabolism
Necroptosis
Neuroinflammatory Diseases
Apoptosis
Necrosis
Caspase 1
/ metabolism
Receptors, Death Domain
/ metabolism
Interleukin-1
/ metabolism
Receptor-Interacting Protein Serine-Threonine Kinases
/ genetics
MicroRNAs
NDDs
NLRP3 inflammasome
Neuronal necroptosis
RIPK/MLKL necrosome
Viral infection
miRs
Journal
Biochemical pharmacology
ISSN: 1873-2968
Titre abrégé: Biochem Pharmacol
Pays: England
ID NLM: 0101032
Informations de publication
Date de publication:
07 2023
07 2023
Historique:
received:
17
03
2023
revised:
09
05
2023
accepted:
10
05
2023
medline:
19
6
2023
pubmed:
18
5
2023
entrez:
17
5
2023
Statut:
ppublish
Résumé
Neuronal necroptosis (programmed necrosis) in the CNS naturally occurs through a caspase-independent way and, especially in neurodegenerative diseases (NDDs) such as Alzheimer's disease (AD), Parknson's disease (PD), Amyotrophic Lateral Sclerosis (ALS) and viral infections. Understanding necroptosis pathways (death receptor-dependent and independent), and its connections with other cell death pathways could lead to new insights into treatment. Receptor-interacting protein kinase (RIPK) mediates necroptosis via mixed-lineage kinase-like (MLKL) proteins. RIPK/MLKL necrosome contains FADD, procaspase-8-cellular FLICE-inhibitory proteins (cFLIPs), RIPK1/RIPK3, and MLKL. The necrotic stimuli cause phosphorylation of MLKL and translocate to the plasma membrane, causing an influx of Ca
Identifiants
pubmed: 37196683
pii: S0006-2952(23)00182-X
doi: 10.1016/j.bcp.2023.115591
pii:
doi:
Substances chimiques
Protein Kinases
EC 2.7.-
Inflammasomes
0
NLR Family, Pyrin Domain-Containing 3 Protein
0
Caspase 1
EC 3.4.22.36
Receptors, Death Domain
0
Interleukin-1
0
Receptor-Interacting Protein Serine-Threonine Kinases
EC 2.7.11.1
MIRN512 microRNA, human
0
MicroRNAs
0
MIRN874 microRNA, human
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
115591Informations de copyright
Copyright © 2023 Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.