The Ca
Ca2+/calmodulin-dependent protein kinase II
cardiovascular disease
cell biology
left ventricular hypertrophy
mechanosensitive channels
medicine
mouse
Journal
eLife
ISSN: 2050-084X
Titre abrégé: Elife
Pays: England
ID NLM: 101579614
Informations de publication
Date de publication:
30 06 2021
30 06 2021
Historique:
received:
15
01
2021
accepted:
20
06
2021
entrez:
30
6
2021
pubmed:
1
7
2021
medline:
9
10
2021
Statut:
epublish
Résumé
Pathological left ventricular hypertrophy (LVH) occurs in response to pressure overload and remains the single most important clinical predictor of cardiac mortality. The molecular pathways in the induction of pressure overload LVH are potential targets for therapeutic intervention. Current treatments aim to remove the pressure overload stimulus for LVH, but do not completely reverse adverse cardiac remodelling. Although numerous molecular signalling steps in the induction of LVH have been identified, the initial step by which mechanical stretch associated with cardiac pressure overload is converted into a chemical signal that initiates hypertrophic signalling remains unresolved. In this study, we show that selective deletion of transient receptor potential melastatin 4 (TRPM4) channels in mouse cardiomyocytes results in an approximately 50% reduction in the LVH induced by transverse aortic constriction. Our results suggest that TRPM4 channel is an important component of the mechanosensory signalling pathway that induces LVH in response to pressure overload and represents a potential novel therapeutic target for the prevention of pathological LVH.
Identifiants
pubmed: 34190686
doi: 10.7554/eLife.66582
pii: 66582
pmc: PMC8245133
doi:
pii:
Substances chimiques
TRPM Cation Channels
0
TRPM4 protein, mouse
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : National Health and Medical Research Council
ID : APP1108013
Organisme : National Health and Medical Research Council
ID : APP1135974
Organisme : Fonds Wetenschappelijk Onderzoek
ID : G0E0317N
Organisme : KU Leuven
ID : TRPLe
Organisme : NSW Health
ID : EMCRFellowship
Informations de copyright
© 2021, Guo et al.
Déclaration de conflit d'intérêts
YG, ZY, JW, HG, SK, SI, AC, SH, SP, AP, CC, RG, RV, MF, BM No competing interests declared
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