The release and activity of HMGB1 in ferroptosis.
Animals
Autophagy
Carbolines
/ pharmacology
Cell Death
Cell Line, Tumor
Chloroquine
/ pharmacology
Ferritins
/ metabolism
Fibroblasts
/ metabolism
HMGB1 Protein
/ metabolism
Humans
Immunity, Innate
Inflammation
Iron Overload
Lipid Peroxidation
Macrolides
/ pharmacology
Mice
Neoplasms
Oximes
/ pharmacology
Piperazines
/ pharmacology
Sorafenib
/ pharmacology
Sulfonamides
/ pharmacology
Toll-Like Receptor 4
/ metabolism
AGER
Autophagy
DAMP
Ferroptosis
HMGB1
Inflammation
Journal
Biochemical and biophysical research communications
ISSN: 1090-2104
Titre abrégé: Biochem Biophys Res Commun
Pays: United States
ID NLM: 0372516
Informations de publication
Date de publication:
05 03 2019
05 03 2019
Historique:
received:
08
01
2019
accepted:
18
01
2019
pubmed:
29
1
2019
medline:
13
11
2019
entrez:
29
1
2019
Statut:
ppublish
Résumé
Damage-associated molecular pattern molecules (DAMPs) are endogenous danger signals that alert the innate immune system and shape the inflammation response to cell death. However, the release and activity of DAMPs in ferroptosis, a recently identified form of regulated necrosis characterized by iron overload and lipid peroxidation, still remain poorly understood. Here, we demonstrate that HMGB1 is a DAMP released by ferroptotic cells in an autophagy-dependent manner. Both type I and II ferroptosis activators, including erastin, sorafenib, RSL3, and FIN56, induce HMGB1 release in cancer and noncancer cells. In contrast, genetic ablation (using ATG5
Identifiants
pubmed: 30686534
pii: S0006-291X(19)30103-2
doi: 10.1016/j.bbrc.2019.01.090
pii:
doi:
Substances chimiques
Carbolines
0
FIN56 compound
0
HMGB1 Protein
0
HMGB1 protein, human
0
HMGB1 protein, mouse
0
Macrolides
0
Oximes
0
Piperazines
0
RSL3 compound
0
Sulfonamides
0
TLR4 protein, human
0
Toll-Like Receptor 4
0
erastin
0
Chloroquine
886U3H6UFF
bafilomycin A1
88899-55-2
Ferritins
9007-73-2
Sorafenib
9ZOQ3TZI87
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
278-283Informations de copyright
Copyright © 2019 Elsevier Inc. All rights reserved.