ACSL4 is essential for radiation-induced intestinal injury by initiating ferroptosis.
Journal
Cell death discovery
ISSN: 2058-7716
Titre abrégé: Cell Death Discov
Pays: United States
ID NLM: 101665035
Informations de publication
Date de publication:
22 Jul 2022
22 Jul 2022
Historique:
received:
27
01
2022
accepted:
11
07
2022
revised:
07
07
2022
entrez:
22
7
2022
pubmed:
23
7
2022
medline:
23
7
2022
Statut:
epublish
Résumé
Lipid peroxidation-induced ferroptosis is a newly recognized type of programmed cell death. With the method of RNA sequencing, we found that irradiation (IR) markedly increased the expression of ferroptosis promotive genes, whereas reduced the expression of ferroptosis suppressive genes in murine intestine tissues, when compared with those of liver and lung tissues. By using ferroptosis inducer RSL-3 and inhibitor liproxstatin-1, we found that ferroptosis is essential for IR-induced intestinal injury. Acyl-CoA Synthetase Long-Chain Family Member 4 (ACSL4) is an important component for ferroptosis execution, and we found that ACSL4 expression was significantly upregulated in irradiated intestine tissues, but not in liver or lung tissues. Antibacterial and antifungal regents reduced the expression of ASCL4 and protected against tissue injury in irradiated intestine tissues. Further studies showed that troglitazone, a ACSL4 inhibitor, succeeded to suppresses intestine lipid peroxidation and tissue damage after IR.
Identifiants
pubmed: 35869042
doi: 10.1038/s41420-022-01127-w
pii: 10.1038/s41420-022-01127-w
pmc: PMC9307849
doi:
Types de publication
Journal Article
Langues
eng
Pagination
332Informations de copyright
© 2022. The Author(s).
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