The role of A-kinase anchoring proteins in cardiac oxidative stress.

Détails

Ressource 1Demande d'une copie Sous embargo indéterminé.
Etat: Public
Version: Final published version
Licence: CC BY-NC-ND 4.0
ID Serval
serval:BIB_5BFC10C47572
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Titre
The role of A-kinase anchoring proteins in cardiac oxidative stress.
Périodique
Biochemical Society transactions
Auteur(s)
Diviani D., Osman H., Delaunay M., Kaiser S.
ISSN
1470-8752 (Electronic)
ISSN-L
0300-5127
Statut éditorial
Publié
Date de publication
31/10/2019
Peer-reviewed
Oui
Volume
47
Numéro
5
Pages
1341-1353
Langue
anglais
Notes
Publication types: Journal Article
Publication Status: ppublish
Résumé
Cardiac stress initiates a pathological remodeling process that is associated with cardiomyocyte loss and fibrosis that ultimately leads to heart failure. In the injured heart, a pathologically elevated synthesis of reactive oxygen species (ROS) is the main driver of oxidative stress and consequent cardiomyocyte dysfunction and death. In this context, the cAMP-dependent protein kinase (PKA) plays a central role in regulating signaling pathways that protect the heart against ROS-induced cardiac damage. In cardiac cells, spatiotemporal regulation of PKA activity is controlled by A-kinase anchoring proteins (AKAPs). This family of scaffolding proteins tether PKA and other transduction enzymes at subcellular microdomains where they can co-ordinate cellular responses regulating oxidative stress. In this review, we will discuss recent literature illustrating the role of PKA and AKAPs in modulating the detrimental impact of ROS production on cardiac function.
Mots-clé
A-kinase anchoring protein, cardiac remodeling, cardiomyocyte, cyclic AMP, protein kinase A
Pubmed
Web of science
Open Access
Oui
Financement(s)
Fonds national suisse / Projets / 31003A_175838
Création de la notice
04/01/2020 12:55
Dernière modification de la notice
17/01/2020 6:26
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