Augmented O-GlcNAcylation attenuates intermittent hypoxia-induced cardiac remodeling through the suppression of NFAT and NF-κB activities in mice.
Acylation
Animals
Cell Line
Diabetes Mellitus, Type 2
/ complications
Echocardiography
Glycogen Synthase Kinase 3 beta
/ metabolism
HEK293 Cells
Humans
Hypoxia
/ pathology
Mice
Mice, Transgenic
Myocardium
/ metabolism
N-Acetylglucosaminyltransferases
/ genetics
NF-kappa B
/ metabolism
NFATC Transcription Factors
/ metabolism
Oxidative Stress
Phosphorylation
Ventricular Remodeling
GSK-3β
NF-κB
NFAT
O-GlcNAcylation
cardiac remodeling
Journal
Hypertension research : official journal of the Japanese Society of Hypertension
ISSN: 1348-4214
Titre abrégé: Hypertens Res
Pays: England
ID NLM: 9307690
Informations de publication
Date de publication:
12 2019
12 2019
Historique:
received:
01
03
2019
accepted:
03
07
2019
revised:
04
06
2019
pubmed:
15
8
2019
medline:
5
11
2020
entrez:
15
8
2019
Statut:
ppublish
Résumé
Type 2 diabetes mellitus (T
Identifiants
pubmed: 31409917
doi: 10.1038/s41440-019-0311-x
pii: 10.1038/s41440-019-0311-x
doi:
Substances chimiques
NF-kappa B
0
NFATC Transcription Factors
0
N-Acetylglucosaminyltransferases
EC 2.4.1.-
UDP-N-acetylglucosamine-peptide beta-N-acetylglucosaminyltransferase
EC 2.4.1.-
Glycogen Synthase Kinase 3 beta
EC 2.7.11.1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1858-1871Commentaires et corrections
Type : CommentIn
Références
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