Targeting necroptosis in fibrosis.
Fibrosis
MLKL
Necroptosis
RIPK1
RIPK3
Journal
Molecular biology reports
ISSN: 1573-4978
Titre abrégé: Mol Biol Rep
Pays: Netherlands
ID NLM: 0403234
Informations de publication
Date de publication:
Dec 2023
Dec 2023
Historique:
received:
14
08
2023
accepted:
27
09
2023
medline:
27
11
2023
pubmed:
1
11
2023
entrez:
1
11
2023
Statut:
ppublish
Résumé
Necroptosis, a type of programmed cell death that resembles necrosis, is now known to depend on a different molecular mechanism from apoptosis, according to several recent studies. Many efforts have reported the possible influence of necroptosis in human disorders and concluded the crucial role in the pathophysiology of various diseases, including liver diseases, renal injuries, cancers, and others. Fibrosis is the most common end-stage pathological cascade of several chronic inflammatory disorders. In this review, we explain the impact of necroptosis and fibrosis, for which necroptosis has been demonstrated to be a contributing factor. We also go over the inhibitors of necroptosis and how they have been applied to fibrosis models. This review helps to clarify the role of necroptosis in fibrosis and will encourage clinical efforts to target this pathway of programmed cell death.
Identifiants
pubmed: 37910384
doi: 10.1007/s11033-023-08857-9
pii: 10.1007/s11033-023-08857-9
pmc: PMC10676318
doi:
Substances chimiques
Protein Kinases
EC 2.7.-
Receptor-Interacting Protein Serine-Threonine Kinases
EC 2.7.11.1
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
10471-10484Informations de copyright
© 2023. The Author(s).
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