The Role of Cyclic AMP Signaling in Cardiac Fibrosis.

Détails

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Etat: Public
Version: Final published version
Licence: CC BY 4.0
ID Serval
serval:BIB_526A7E1D4BEC
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 Cyclic AMP Signaling in Cardiac Fibrosis.
Périodique
Cells
Auteur(s)
Delaunay M., Osman H., Kaiser S., Diviani D.
ISSN
2073-4409 (Electronic)
ISSN-L
2073-4409
Statut éditorial
Publié
Date de publication
26/12/2019
Peer-reviewed
Oui
Volume
9
Numéro
1
Langue
anglais
Notes
Publication types: Journal Article ; Review
Publication Status: epublish
Résumé
Myocardial stress and injury invariably promote remodeling of the cardiac tissue, which is associated with cardiomyocyte death and development of fibrosis. The fibrotic process is initially triggered by the differentiation of resident cardiac fibroblasts into myofibroblasts. These activated fibroblasts display increased proliferative capacity and secrete large amounts of extracellular matrix. Uncontrolled myofibroblast activation can thus promote heart stiffness, cardiac dysfunction, arrhythmias, and progression to heart failure. Despite the well-established role of myofibroblasts in mediating cardiac disease, our current knowledge on how signaling pathways promoting fibrosis are regulated and coordinated in this cell type is largely incomplete. In this respect, cyclic adenosine monophosphate (cAMP) signaling acts as a major modulator of fibrotic responses activated in fibroblasts of injured or stressed hearts. In particular, accumulating evidence now suggests that upstream cAMP modulators including G protein-coupled receptors, adenylyl cyclases (ACs), and phosphodiesterases (PDEs); downstream cAMP effectors such as protein kinase A (PKA) and the guanine nucleotide exchange factor Epac; and cAMP signaling organizers such as A-kinase anchoring proteins (AKAPs) modulate a variety of fundamental cellular processes involved in myocardial fibrosis including myofibroblast differentiation, proliferation, collagen secretion, and invasiveness. The current review will discuss recent advances highlighting the role of cAMP and AKAP-mediated signaling in regulating pathophysiological responses controlling cardiac fibrosis.
Mots-clé
A-kinase anchoring protein (AKAP), adenylyl cyclase, cardiac fibrosis, cardiac remodeling, cyclic AMP, phosphodiesterase, protein kinase A
Pubmed
Open Access
Oui
Financement(s)
Fonds national suisse / Projets / 31003A_175838
Création de la notice
03/01/2020 21:27
Dernière modification de la notice
17/01/2020 6:26
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