Epac Function and cAMP Scaffolds in the Heart and Lung
1
Inserm UMR-1048, Institut des Maladies Métaboliques et Cardiovasculaires, Université Toulouse III, 31432 Toulouse, France
2
Department of Molecular Pharmacology, University of Groningen, 9713AV Groningen, The Netherlands
3
Groningen Research Institute for Asthma and COPD (GRIAC), University Medical Center Groningen, University of Groningen, 9713AV Groningen, The Netherlands
*
Author to whom correspondence should be addressed.
†
These authors contributed equally to this work.
J. Cardiovasc. Dev. Dis. 2018, 5(1), 9; https://doi.org/10.3390/jcdd5010009
Received: 12 January 2018 / Revised: 25 January 2018 / Accepted: 29 January 2018 / Published: 3 February 2018
(This article belongs to the Special Issue Cyclic Nucleotide Signaling and the Cardiovascular System)
Evidence collected over the last ten years indicates that Epac and cAMP scaffold proteins play a critical role in integrating and transducing multiple signaling pathways at the basis of cardiac and lung physiopathology. Some of the deleterious effects of Epac, such as cardiomyocyte hypertrophy and arrhythmia, initially described in vitro, have been confirmed in genetically modified mice for Epac1 and Epac2. Similar recent findings have been collected in the lung. The following sections will describe how Epac and cAMP signalosomes in different subcellular compartments may contribute to cardiac and lung diseases.
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MDPI and ACS Style
Laudette, M.; Zuo, H.; Lezoualc’h, F.; Schmidt, M. Epac Function and cAMP Scaffolds in the Heart and Lung. J. Cardiovasc. Dev. Dis. 2018, 5, 9.
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