Inhibited autophagy may contribute to heme toxicity in cardiomyoblast cells.
Autophagy
Cardiomyocytes
Heme
Heme oxygenase-1
Toxicity
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:
16 04 2019
16 04 2019
Historique:
received:
21
02
2019
accepted:
25
02
2019
pubmed:
6
3
2019
medline:
14
1
2020
entrez:
6
3
2019
Statut:
ppublish
Résumé
Several groups have demonstrated that induction of heme-oxygenase-1 (HO-1) could protect the myocardium against ischemic events; however, heme accumulation could lead to toxicity. The aim of the present study was to investigate the role of autophagy in heme toxicity. H9c2 cardiomyoblast cells were treated with different dose of hemin or cobalt-protoporphyrin IX (CoPP
Identifiants
pubmed: 30833080
pii: S0006-291X(19)30341-9
doi: 10.1016/j.bbrc.2019.02.140
pii:
doi:
Substances chimiques
Protoporphyrins
0
Reactive Oxygen Species
0
cobaltiprotoporphyrin
63AAN3JDZE
Hemin
743LRP9S7N
Heme Oxygenase-1
EC 1.14.14.18
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
732-738Informations de copyright
Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.