Pressure overload inhibits glucocorticoid receptor transcriptional activity in cardiomyocytes and promotes pathological cardiac hypertrophy.


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
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

122-130

Informations de copyright

Copyright © 2019. Published by Elsevier Ltd.

Auteurs

Tomohiro Matsuhashi (T)

Department of Cardiology, Keio University School of Medicine, Tokyo, Japan.

Jin Endo (J)

Department of Cardiology, Keio University School of Medicine, Tokyo, Japan.

Yoshinori Katsumata (Y)

Department of Cardiology, Keio University School of Medicine, Tokyo, Japan.

Tsunehisa Yamamoto (T)

Department of Cardiology, Keio University School of Medicine, Tokyo, Japan.

Noriaki Shimizu (N)

Division of Rheumatology, Center for Antibody and Vaccine Therapy, IMSUT Hospital, Institute of Medical Science University of Tokyo, Tokyo, Japan.

Noritada Yoshikawa (N)

Division of Rheumatology, Center for Antibody and Vaccine Therapy, IMSUT Hospital, Institute of Medical Science University of Tokyo, Tokyo, Japan.

Masaharu Kataoka (M)

Department of Cardiology, Keio University School of Medicine, Tokyo, Japan.

Sarasa Isobe (S)

Department of Cardiology, Keio University School of Medicine, Tokyo, Japan.

Hidenori Moriyama (H)

Department of Cardiology, Keio University School of Medicine, Tokyo, Japan.

Shinichi Goto (S)

Department of Cardiology, Keio University School of Medicine, Tokyo, Japan.

Keiichi Fukuda (K)

Department of Cardiology, Keio University School of Medicine, Tokyo, Japan.

Hirotoshi Tanaka (H)

Division of Rheumatology, Center for Antibody and Vaccine Therapy, IMSUT Hospital, Institute of Medical Science University of Tokyo, Tokyo, Japan.

Motoaki Sano (M)

Department of Cardiology, Keio University School of Medicine, Tokyo, Japan. Electronic address: msano@a8.keio.jp.

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Classifications MeSH