Molecular Insights into the Mechanism of Necroptosis: The Necrosome As a Potential Therapeutic Target.
MLKL
RIP kinase
cancer
inflammatory diseases
necroptosis
necrosome
programmed cell death
Journal
Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052
Informations de publication
Date de publication:
21 11 2019
21 11 2019
Historique:
received:
30
10
2019
revised:
13
11
2019
accepted:
19
11
2019
entrez:
27
11
2019
pubmed:
27
11
2019
medline:
18
8
2020
Statut:
epublish
Résumé
Necroptosis, or regulated necrosis, is an important type of programmed cell death in addition to apoptosis. Necroptosis induction leads to cell membrane disruption, inflammation and vascularization. It plays important roles in various pathological processes, including neurodegeneration, inflammatory diseases, multiple cancers, and kidney injury. The molecular regulation of necroptotic pathway has been intensively studied in recent years. Necroptosis can be triggered by multiple stimuli and this pathway is regulated through activation of receptor-interacting protein kinase 1 (RIPK1), RIPK3 and pseudokinase mixed lineage kinase domain-like (MLKL). A better understanding of the mechanism of regulation of necroptosis will further aid to the development of novel drugs for necroptosis-associated human diseases. In this review, we focus on new insights in the regulatory machinery of necroptosis. We further discuss the role of necroptosis in different pathologies, its potential as a therapeutic target and the current status of clinical development of drugs interfering in the necroptotic pathway.
Identifiants
pubmed: 31766571
pii: cells8121486
doi: 10.3390/cells8121486
pmc: PMC6952807
pii:
doi:
Substances chimiques
MLKL protein, human
EC 2.7.-
Protein Kinases
EC 2.7.-
RIPK1 protein, human
EC 2.7.11.1
RIPK3 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, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Déclaration de conflit d'intérêts
The authors declare that no conflicts of interest.
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