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Home All issues Volume 31 / No 10 (Octobre 2015) Med Sci (Paris), 31 10 (2015) 881-888 References
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Issue
Med Sci (Paris)
Volume 31, Number 10, Octobre 2015
Page(s) 881 - 888
Section M/S Revues
DOI https://doi.org/10.1051/medsci/20153110014
Published online 19 October 2015
  1. Kemi OJ, Haram PM, Loennechen JP, et al. Moderate versus high exercise intensity: differential effects on aerobic fitness, cardiomyocyte contractility, and endothelial function. Cardiovasc Res 2005 ; 67 : 161–172. [CrossRef] [PubMed] [Google Scholar]
  2. Katz AM. Cardiomyopathy of overload. A major determinant of prognosis in congestive heart failure. N Engl J Med 1990 ; 322 : 100–110. [CrossRef] [PubMed] [Google Scholar]
  3. Levy D, Garrison RJ, Savage DD, et al. Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study. N Engl J Med 1990 ; 322 : 1561–1566. [CrossRef] [PubMed] [Google Scholar]
  4. Zannad F, Alla F, Dousset B, et al. Limitation of excessive extracellular matrix turnover may contribute to survival benefit of spironolactone therapy in patients with congestive heart failure: insights from the randomized aldactone evaluation study (RALES). Rales investigators. Circulation 2000 ; 102 : 2700–2706. [CrossRef] [Google Scholar]
  5. Swynghedauw B.. Molecular mechanisms of myocardial remodeling. Physiol Rev 1999 ; 79 : 215–262. [PubMed] [Google Scholar]
  6. Molkentin JD, Lu JR, Antos CL, et al. A calcineurin-dependent transcriptional pathway for cardiac hypertrophy. Cell 1998 ; 93 : 215–228. [CrossRef] [PubMed] [Google Scholar]
  7. Passier R, Zeng H, Frey N, et al. CaM kinase signaling induces cardiac hypertrophy and activates the MEF2 transcription factor in vivo. J Clin Invest 2000 ; 105 : 1395–1406. [CrossRef] [PubMed] [Google Scholar]
  8. Loyer X, Gómez AM, Milliez P, et al. Cardiomyocyte overexpression of neuronal nitric oxide synthase delays transition toward heart failure in response to pressure overload by preserving calcium cycling. Circulation 2008 ; 117 : 3187–3198. [CrossRef] [PubMed] [Google Scholar]
  9. Koitabashi N, Danner T, Zaiman AL, et al. Pivotal role of cardiomyocyte TGF-β signaling in the murine pathological response to sustained pressure overload. J Clin Invest 2011 ; 121 : 2301–2312. [CrossRef] [PubMed] [Google Scholar]
  10. van Berlo JH, Maillet M, Molkentin JD. Signaling effectors underlying pathologic growth and remodeling of the heart. J Clin Invest 2013 ; 123 : 37–45. [CrossRef] [PubMed] [Google Scholar]
  11. Maillet M, van Berlo JH, Molkentin JD. Molecular basis of physiological heart growth: fundamental concepts and new players. Nat Rev Mol Cell Biol 2013 ; 14 : 38–48. [CrossRef] [PubMed] [Google Scholar]
  12. Movsesian MA, Bristow MR. Alterations in cAMP-mediated signaling and their role in the pathophysiology of dilated cardiomyopathy. Curr Top Dev Biol 2005 ; 68 : 25–48. [CrossRef] [PubMed] [Google Scholar]
  13. Bristow MR. Treatment of chronic heart failure with β-adrenergic receptor antagonists: a convergence of receptor pharmacology and clinical cardiology. Circ Res 2011 ; 109 : 1176–1194. [CrossRef] [PubMed] [Google Scholar]
  14. Perrino C, Naga Prasad S V, Schroder JN, et al. Restoration of beta-adrenergic receptor signaling and contractile function in heart failure by disruption of the betaARK1/phosphoinositide 3-kinase complex. Circulation 2005 ; 111 : 2579–2587. [CrossRef] [PubMed] [Google Scholar]
  15. Métayé T, Perdrisot R, Kraimps JL. GRK et arrestines : la piste thérapeutique ? Med Sci (Paris) 2006 ; 22 : 537–543. [CrossRef] [EDP Sciences] [PubMed] [Google Scholar]
  16. Berthouze M, Laurent AC, Breckler M, et al. New perspectives in cAMP-signaling modulation. Curr Heart Fail Rep 2011 ; 8 : 159–167. [CrossRef] [PubMed] [Google Scholar]
  17. Mika D, Leroy J, Fischmeister R, et al. Rôle des phosphodiestérases des nucléotides cycliques de types 3 et 4 dans le couplage excitation-contraction et les arythmies cardiaques. Med Sci (Paris) 2013 ; 29 : 617–622. [CrossRef] [EDP Sciences] [PubMed] [Google Scholar]
  18. de Rooij J, Zwartkruis FJ, Verheijen MH, et al. Epac is a Rap1 guanine-nucleotide-exchange factor directly activated by cyclic AMP. Nature 1998 ; 396 : 474–477. [CrossRef] [PubMed] [Google Scholar]
  19. Kawasaki H, Springett GM, Mochizuki N, et al. A family of cAMP-binding proteins that directly activate Rap1. Science 1998 ; 282 : 2275–2279. [CrossRef] [PubMed] [Google Scholar]
  20. Rehmann H, Schwede F, Døskeland SO, et al. Ligand-mediated activation of the cAMP-responsive guanine nucleotide exchange factor Epac. J Biol Chem 2003 ; 278 : 38548–38556. [CrossRef] [PubMed] [Google Scholar]
  21. Enserink JM, Christensen AE, De Rooij J, et al. A novel Epac-specific cAMP analogue demonstrates independent regulation of Rap1 and ERK. Nat Cell Biol 2002 ; 4 : 901–906. [CrossRef] [PubMed] [Google Scholar]
  22. Morel E, Marcantoni A, Gastineau M, et al. cAMP-binding protein Epac induces cardiomyocyte hypertrophy. Circ Res 2005 ; 97 : 1296–1304. [CrossRef] [PubMed] [Google Scholar]
  23. Métrich M, Lucas A, Gastineau M, et al. Epac mediates beta-adrenergic receptor-induced cardiomyocyte hypertrophy. Circ Res 2008 ; 102 : 959–965. [CrossRef] [PubMed] [Google Scholar]
  24. Courilleau D, Bisserier M, Jullian JC, et al. Identification of a tetrahydroquinoline analog as a pharmacological inhibitor of the cAMP-binding protein Epac. J Biol Chem 2012 ; 287 : 44192–44202. [CrossRef] [PubMed] [Google Scholar]
  25. Bisserier M, Blondeau JP. Lezoualc’h F. Epac proteins: specific ligands and role in cardiac remodelling. Biochem Soc Trans 2014 ; 42 : 257–264. [CrossRef] [PubMed] [Google Scholar]
  26. Métrich M, Laurent AC, Breckler M, et al. Epac activation induces histone deacetylase nuclear export via a Ras-dependent signalling pathway. Cell Signal 2010 ; 22 : 1459–1468. [CrossRef] [PubMed] [Google Scholar]
  27. Pereira L, Ruiz-Hurtado G, Morel E, et al. Epac enhances excitation-transcription coupling in cardiac myocytes. J Mol Cell Cardiol 2012 ; 52 : 283–291. [CrossRef] [PubMed] [Google Scholar]
  28. Berthouze-Duquesnes M, Lucas A, Saulière A, et al. Specific interactions between Epac1, β-arrestin2 and PDE4D5 regulate β-adrenergic receptor subtype differential effects on cardiac hypertrophic signaling. Cell Signal 2013 ; 25 : 970–980. [CrossRef] [PubMed] [Google Scholar]
  29. Pereira L, Cheng H, Lao DH, et al. Epac2 mediates cardiac β1-adrenergic-dependent sarcoplasmic reticulum Ca2+ leak and arrhythmia. Circulation 2013 ; 127 : 913–922. [CrossRef] [PubMed] [Google Scholar]
  30. Okumura S, Fujita T, Cai W, et al. Epac1-dependent phospholamban phosphorylation mediates the cardiac response to stresses. J Clin Invest 2014 ; 124 : 2785–2801. [CrossRef] [PubMed] [Google Scholar]
  31. Laurent AC, Bisserier M, Lucas A, et al. Exchange protein directly activated by cAMP 1 promotes autophagy during cardiomyocyte hypertrophy. Cardiovasc Res 2015 ; 105 : 55–64. [CrossRef] [PubMed] [Google Scholar]
  32. Lacampagne A, Fauconnier J, Richard S. Récepteur de la ryanodine et dysfonctionnement myocardique. Med Sci (Paris) 2008 ; 24 : 399–405. [CrossRef] [EDP Sciences] [PubMed] [Google Scholar]
  33. Pereira L, Métrich M, Fernández-Velasco M, et al. The cAMP binding protein Epac modulates Ca2+ sparks by a Ca2+/calmodulin kinase signalling pathway in rat cardiac myocytes. J Physiol 2007 ; 583 : 685–694. [CrossRef] [PubMed] [Google Scholar]
  34. Oestreich EA, Malik S, Goonasekera SA, et al. Epac and phospholipase Cepsilon regulate Ca2+ release in the heart by activation of protein kinase Cepsilon and calcium-calmodulin kinase II. J Biol Chem 2009 ; 284 : 1514–1522. [CrossRef] [PubMed] [Google Scholar]
  35. Hothi SS, Gurung IS, Heathcote JC, et al. Epac activation, altered calcium homeostasis and ventricular arrhythmogenesis in the murine heart. Pflugers Arch 2008 ; 457 : 253–270. [CrossRef] [PubMed] [Google Scholar]
  36. Leenders JJ, Pinto YM, Creemers EE. Tapping the brake on cardiac growth-endogenous repressors of hypertrophic signaling. J Mol Cell Cardiol 2011 ; 51 : 156–167. [CrossRef] [PubMed] [Google Scholar]
  37. Pan F, Sun L, Kardian DB, et al. Feedback inhibition of calcineurin and Ras by a dual inhibitory protein Carabin. Nature 2007 ; 445 : 433–436. [CrossRef] [PubMed] [Google Scholar]
  38. Schickel JN, Pasquali JL, Soley A, et al. Carabin deficiency in B cells increases BCR-TLR9 costimulation-induced autoimmunity. EMBO Mol Med 2012 ; 4 : 1261–1275. [CrossRef] [PubMed] [Google Scholar]
  39. Bisserier M, Berthouze-Duquesnes M, Breckler M, et al. Carabin protects against cardiac hypertrophy by blocking calcineurin, Ras, and Ca2+/calmodulin-dependent protein kinase II signaling. Circulation 2015 ; 131 : 390–400. [CrossRef] [PubMed] [Google Scholar]
  40. Lyon RC, Zanella F, Omens JH, et al. Mechanotransduction in cardiac hypertrophy and failure. Circ Res 2015 ; 116 : 1462–1476. [CrossRef] [PubMed] [Google Scholar]
  41. Pinet F, Bauters C. Potentieldes ARN non-codants comme biomarqueurs dans l’insuffisance cardiaque. Med Sci (Paris) 2015 ; 31 : 770–776. [CrossRef] [EDP Sciences] [PubMed] [Google Scholar]

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