The inotropic and arrhythmogenic effects of acutely increased late I
CaMKII
L-type Ca2+ current (ICa)
PKARIα
excitation contraction coupling (ECC)
oxidative stress
Journal
Frontiers in cardiovascular medicine
ISSN: 2297-055X
Titre abrégé: Front Cardiovasc Med
Pays: Switzerland
ID NLM: 101653388
Informations de publication
Date de publication:
2024
2024
Historique:
received:
31
01
2024
accepted:
10
06
2024
medline:
30
7
2024
pubmed:
30
7
2024
entrez:
30
7
2024
Statut:
epublish
Résumé
Acute stimulation of the late sodium current (I We aimed to investigate whether the increase of the systolic Ca We used a transgenic mouse model in which PKARIα was made resistant to oxidative activation by homozygous knock-in replacement of redox-sensitive Cysteine 17 with Serine within the regulatory subunits of PKARIα (KI). ATX-II (at 1 nmol/L) was used to acutely enhance I ATX-II increased I The inotropic and arrhythmogenic effects of acutely increased I
Sections du résumé
Background
UNASSIGNED
Acute stimulation of the late sodium current (I
Objectives
UNASSIGNED
We aimed to investigate whether the increase of the systolic Ca
Methods
UNASSIGNED
We used a transgenic mouse model in which PKARIα was made resistant to oxidative activation by homozygous knock-in replacement of redox-sensitive Cysteine 17 with Serine within the regulatory subunits of PKARIα (KI). ATX-II (at 1 nmol/L) was used to acutely enhance I
Results
UNASSIGNED
ATX-II increased I
Conclusions
UNASSIGNED
The inotropic and arrhythmogenic effects of acutely increased I
Identifiants
pubmed: 39077112
doi: 10.3389/fcvm.2024.1379930
pmc: PMC11284163
doi:
Types de publication
Journal Article
Langues
eng
Pagination
1379930Informations de copyright
© 2024 Gissibl, Stengel, Tarnowski, Maier, Wagner, Feder and Sag.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.