Iron derived from autophagy-mediated ferritin degradation induces cardiomyocyte death and heart failure in mice.
Animals
Aorta
Autophagy
Cardiomyopathies
/ drug therapy
Constriction
Cyclohexylamines
/ pharmacology
Disease Models, Animal
Ferritins
/ genetics
Heart Failure
/ drug therapy
Iron
/ metabolism
Lipid Peroxidation
Male
Mice, Inbred C57BL
Mice, Transgenic
Myocytes, Cardiac
/ drug effects
Nuclear Receptor Coactivators
/ genetics
Phenylenediamines
/ pharmacology
autophagy
biochemistry
chemical biology
ferritin
heart failure
iron
medicine
mouse
necrosis
Journal
eLife
ISSN: 2050-084X
Titre abrégé: Elife
Pays: England
ID NLM: 101579614
Informations de publication
Date de publication:
02 02 2021
02 02 2021
Historique:
received:
16
08
2020
accepted:
08
01
2021
entrez:
2
2
2021
pubmed:
3
2
2021
medline:
3
2
2022
Statut:
epublish
Résumé
Heart failure is a major public health problem, and abnormal iron metabolism is common in patients with heart failure. Although iron is necessary for metabolic homeostasis, it induces a programmed necrosis. Iron release from ferritin storage is through nuclear receptor coactivator 4 (NCOA4)-mediated autophagic degradation, known as ferritinophagy. However, the role of ferritinophagy in the stressed heart remains unclear. Deletion of
Identifiants
pubmed: 33526170
doi: 10.7554/eLife.62174
pii: 62174
pmc: PMC7853718
doi:
pii:
Substances chimiques
Cyclohexylamines
0
NcoA4 protein, mouse
0
Nuclear Receptor Coactivators
0
Phenylenediamines
0
ferrostatin-1
0
Ferritins
9007-73-2
Iron
E1UOL152H7
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : British Heart Foundation
ID : RE/13/2/30182
Pays : United Kingdom
Organisme : British Heart Foundation
ID : CH/11/3/29051
Pays : United Kingdom
Organisme : British Heart Foundation
ID : CH/1999001/11735
Pays : United Kingdom
Organisme : British Heart Foundation
ID : RG/16/15/32294
Pays : United Kingdom
Informations de copyright
© 2021, Ito et al.
Déclaration de conflit d'intérêts
JI, SO, MR, HU, TM, YT, HA, KN, MA, MT, KN, AS, KO No competing interests declared
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