Necroptosis and RIPK1-mediated neuroinflammation in CNS diseases.
Journal
Nature reviews. Neuroscience
ISSN: 1471-0048
Titre abrégé: Nat Rev Neurosci
Pays: England
ID NLM: 100962781
Informations de publication
Date de publication:
01 2019
01 2019
Historique:
pubmed:
24
11
2018
medline:
18
12
2019
entrez:
24
11
2018
Statut:
ppublish
Résumé
Apoptosis is crucial for the normal development of the nervous system, whereas neurons in the adult CNS are relatively resistant to this form of cell death. However, under pathological conditions, upregulation of death receptor family ligands, such as tumour necrosis factor (TNF), can sensitize cells in the CNS to apoptosis and a form of regulated necrotic cell death known as necroptosis that is mediated by receptor-interacting protein kinase 1 (RIPK1), RIPK3 and mixed lineage kinase domain-like protein (MLKL). Necroptosis promotes further cell death and neuroinflammation in the pathogenesis of several neurodegenerative diseases, including multiple sclerosis, amyotrophic lateral sclerosis, Parkinson disease and Alzheimer disease. In this Review, we outline the evidence implicating necroptosis in these neurological diseases and suggest that targeting RIPK1 might help to inhibit multiple cell death pathways and ameliorate neuroinflammation.
Identifiants
pubmed: 30467385
doi: 10.1038/s41583-018-0093-1
pii: 10.1038/s41583-018-0093-1
pmc: PMC6342007
mid: NIHMS1006317
doi:
Substances chimiques
RIPK1 protein, human
EC 2.7.11.1
Receptor-Interacting Protein Serine-Threonine Kinases
EC 2.7.11.1
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
19-33Subventions
Organisme : NIA NIH HHS
ID : R01 AG047231
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS082257
Pays : United States
Organisme : NIA NIH HHS
ID : R21 AG059073
Pays : United States
Organisme : NIA NIH HHS
ID : RF1 AG055521
Pays : United States
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