Pressure overload inhibits glucocorticoid receptor transcriptional activity in cardiomyocytes and promotes pathological cardiac hypertrophy.
Cardiac hypertrophy
Glucocorticoid receptor
Heart failure
KLF15
Mineral corticoid receptor
mTORC1
Journal
Journal of molecular and cellular cardiology
ISSN: 1095-8584
Titre abrégé: J Mol Cell Cardiol
Pays: England
ID NLM: 0262322
Informations de publication
Date de publication:
05 2019
05 2019
Historique:
received:
10
12
2018
revised:
07
02
2019
accepted:
25
03
2019
pubmed:
5
4
2019
medline:
18
6
2020
entrez:
5
4
2019
Statut:
ppublish
Résumé
Glucocorticoid receptor (GR) is abundantly expressed in cardiomyocytes. However, the role of GR in regulating cardiac hypertrophy and heart failure in response to pressure overload remains unclear. Cardiomyocyte-specific GR knockout (GRcKO) mice, mineralocorticoid receptor (MR) knockout (MRcKO), and GR and MR double KO (GRMRdcKO) mice were generated using the Cre-lox system. In response to pressure overload, GRcKO mice displayed worse cardiac remodeling compared to control (GR
Identifiants
pubmed: 30946837
pii: S0022-2828(18)31242-2
doi: 10.1016/j.yjmcc.2019.03.019
pii:
doi:
Substances chimiques
Receptors, Glucocorticoid
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
122-130Informations de copyright
Copyright © 2019. Published by Elsevier Ltd.