Turning on cGMP-dependent pathways to treat cardiac dysfunctions: boom, bust, and beyond
Tài liệu tham khảo
Lukowski, 2010, Cardiac hypertrophy is not amplified by deletion of cGMP-dependent protein kinase I in cardiomyocytes, Proc. Natl. Acad. Sci. U.S.A., 107, 5646, 10.1073/pnas.1001360107
Methner, 2013, Protection through postconditioning or a mitochondria-targeted S-nitrosothiol is unaffected by cardiomyocyte-selective ablation of protein kinase G, Basic Res. Cardiol., 108, 337, 10.1007/s00395-013-0337-1
Frantz, 2013, Stress-dependent dilated cardiomyopathy in mice with cardiomyocyte-restricted inactivation of cyclic GMP-dependent protein kinase I, Eur. Heart J., 34, 1233, 10.1093/eurheartj/ehr445
Klaiber, 2011, A cardiac pathway of cyclic GMP-independent signaling of guanylyl cyclase A, the receptor for atrial natriuretic peptide, Proc. Natl. Acad. Sci. U.S.A., 108, 18500, 10.1073/pnas.1103300108
Blanton, 2012, Protein kinase Giα inhibits pressure overload-induced cardiac remodeling and is required for the cardioprotective effect of sildenafil in vivo, J. Am. Heart Assoc., 1, e003731, 10.1161/JAHA.112.003731
Guazzi, 2011, PDE5 inhibition with sildenafil improves left ventricular diastolic function, cardiac geometry, and clinical status in patients with stable systolic heart failure: results of a 1-year, prospective, randomized, placebo-controlled study, Circ. Heart Fail., 4, 8, 10.1161/CIRCHEARTFAILURE.110.944694
van Heerebeek, 2012, Low myocardial protein kinase G activity in heart failure with preserved ejection fraction, Circulation, 126, 830, 10.1161/CIRCULATIONAHA.111.076075
Redfield, 2013, Effect of phosphodiesterase-5 inhibition on exercise capacity and clinical status in heart failure with preserved ejection fraction: a randomized clinical trial, J. Am. Med. Assoc., 309, 1268, 10.1001/jama.2013.2024
Andersen, 2013, Sildenafil and diastolic dysfunction after acute myocardial infarction in patients with preserved ejection fraction: the Sildenafil and Diastolic Dysfunction After Acute Myocardial Infarction (SIDAMI) trial, Circulation, 127, 1200, 10.1161/CIRCULATIONAHA.112.000056
Adamo, 2010, Sildenafil reverses cardiac dysfunction in the mdx mouse model of Duchenne muscular dystrophy, Proc. Natl. Acad. Sci. U.S.A., 107, 19079, 10.1073/pnas.1013077107
Percival, 2012, Sildenafil reduces respiratory muscle weakness and fibrosis in the mdx mouse model of Duchenne muscular dystrophy, J. Pathol., 228, 77, 10.1002/path.4054
Deschepper, 2010, Cardioprotective actions of cyclic GMP: lessons from genetic animal models, Hypertension, 55, 453, 10.1161/HYPERTENSIONAHA.109.145235
Garcia-Dorado, 2009, Myocardial protection against reperfusion injury: the cGMP pathway, Thromb. Haemost., 101, 635, 10.1160/TH08-11-0764
Kass, 2007, Phosphodiesterase type 5: expanding roles in cardiovascular regulation, Circ. Res., 101, 1084, 10.1161/CIRCRESAHA.107.162511
Potter, 2009, Natriuretic peptides: their structures, receptors, physiologic functions and therapeutic applications, Handb. Exp. Pharmacol., 191, 341, 10.1007/978-3-540-68964-5_15
Derbyshire, 2009, Biochemistry of soluble guanylate cyclase, Handb. Exp. Pharmacol., 191, 17, 10.1007/978-3-540-68964-5_2
Hofmann, 2005, The biology of cyclic GMP-dependent protein kinases, J. Biol. Chem., 280, 1, 10.1074/jbc.R400035200
Conti, 2007, Biochemistry and physiology of cyclic nucleotide phosphodiesterases: essential components in cyclic nucleotide signaling, Annu. Rev. Biochem., 76, 481, 10.1146/annurev.biochem.76.060305.150444
Worner, 2007, cGMP signals mainly through cAMP kinase in permeabilized murine aorta, Am. J. Physiol. Heart Circ. Physiol., 292, H237, 10.1152/ajpheart.00079.2006
Movsesian, 2011, Phosphodiesterase inhibition in heart failure, 237
Rybalkin, 2003, Cyclic GMP phosphodiesterases and regulation of smooth muscle function, Circ. Res., 93, 280, 10.1161/01.RES.0000087541.15600.2B
Ecker, 1989, Decreased cardiac concentration of cGMP kinase in hypertensive animals. An index for cardiac vascularization?, Circ. Res., 65, 1361, 10.1161/01.RES.65.5.1361
Potter, 2009, Natriuretic peptides: their structures, receptors, physiologic functions and therapeutic applications, Handb. Exp. Pharmacol., 341, 10.1007/978-3-540-68964-5_15
Lopez, 1995, Salt-resistant hypertension in mice lacking the guanylyl cyclase-A receptor for atrial natriuretic peptide, Nature, 378, 65, 10.1038/378065a0
Oliver, 1997, Hypertension, cardiac hypertrophy, and sudden death in mice lacking natriuretic peptide receptor A, Proc. Natl. Acad. Sci. U.S.A., 94, 14730, 10.1073/pnas.94.26.14730
Holtwick, 2003, Pressure-independent cardiac hypertrophy in mice with cardiomyocyte-restricted inactivation of the atrial natriuretic peptide receptor guanylyl cyclase-A, J. Clin. Invest., 111, 1399, 10.1172/JCI17061
Kishimoto, 2001, A genetic model provides evidence that the receptor for atrial natriuretic peptide (guanylyl cyclase-A) inhibits cardiac ventricular myocyte hypertrophy, Proc. Natl. Acad. Sci. U.S.A., 98, 2703, 10.1073/pnas.051625598
Volpe, 2014, Natriuretic peptides in cardiovascular diseases: current use and perspectives, Eur. Heart J., 35, 419, 10.1093/eurheartj/eht466
Greene, 2013, The cGMP signaling pathway as a therapeutic target in heart failure with preserved ejection fraction, J. Am. Heart Assoc., 2, e000536, 10.1161/JAHA.113.000536
Colucci, 2000, Intravenous nesiritide, a natriuretic peptide, in the treatment of decompensated congestive heart failure. Nesiritide Study Group, N. Engl. J. Med., 343, 246, 10.1056/NEJM200007273430403
O’Connor, 2011, Effect of nesiritide in patients with acute decompensated heart failure, N. Engl. J. Med., 365, 32, 10.1056/NEJMoa1100171
Dickey, 2012, Guanylyl cyclase (GC)-A and GC-B activities in ventricles and cardiomyocytes from failed and non-failed human hearts: GC-A is inactive in the failed cardiomyocyte, J. Mol. Cell. Cardiol., 52, 727, 10.1016/j.yjmcc.2011.11.007
Gotz, 2014, Transgenic mice for real-time visualization of cGMP in intact adult cardiomyocytes, Circ. Res., 114, 1235, 10.1161/CIRCRESAHA.114.302437
Sangaralingham, 2011, The aging heart, myocardial fibrosis, and its relationship to circulating C-type natriuretic peptide, Hypertension, 57, 201, 10.1161/HYPERTENSIONAHA.110.160796
Izumiya, 2012, Chronic C-type natriuretic peptide infusion attenuates angiotensin II-induced myocardial superoxide production and cardiac remodeling, Int. J. Vasc. Med., 2012, 246058
Soeki, 2005, C-type natriuretic peptide, a novel antifibrotic and antihypertrophic agent, prevents cardiac remodeling after myocardial infarction, J. Am. Coll. Cardiol., 45, 608, 10.1016/j.jacc.2004.10.067
Hobbs, 2004, Natriuretic peptide receptor-C regulates coronary blood flow and prevents myocardial ischemia/reperfusion injury: novel cardioprotective role for endothelium-derived C-type natriuretic peptide, Circulation, 110, 1231, 10.1161/01.CIR.0000141802.29945.34
Kilic, 2010, A novel chimeric natriuretic peptide reduces cardiomyocyte hypertrophy through the NHE-1-calcineurin pathway, Cardiovasc. Res., 88, 434, 10.1093/cvr/cvq254
Martin, 2012, CD-NP: a novel engineered dual guanylyl cyclase activator with anti-fibrotic actions in the heart, PLoS ONE, 7, e52422, 10.1371/journal.pone.0052422
Bice, 2014, NO-independent stimulation or activation of soluble guanylyl cyclase during early reperfusion limits infarct size, Cardiovasc. Res., 101, 220, 10.1093/cvr/cvt257
Salloum, 2012, Cinaciguat, a novel activator of soluble guanylate cyclase, protects against ischemia/reperfusion injury: role of hydrogen sulfide, Am. J. Physiol. Heart Circ. Physiol., 302, H1347, 10.1152/ajpheart.00544.2011
Krieg, 2009, BAY 58-2667, a nitric oxide-independent guanylyl cyclase activator, pharmacologically post-conditions rabbit and rat hearts, Eur. Heart J., 30, 1607, 10.1093/eurheartj/ehp143
Irvine, 2012, The soluble guanylyl cyclase activator BAY 58-2667 selectively limits cardiomyocyte hypertrophy, PLoS ONE, 7, e44481, 10.1371/journal.pone.0044481
Groneberg, 2013, Cell-specific deletion of nitric oxide-sensitive guanylyl cyclase reveals a dual pathway for nitrergic neuromuscular transmission in the murine fundus, Gastroenterology, 145, 188, 10.1053/j.gastro.2013.03.042
Groneberg, 2010, Smooth muscle-specific deletion of nitric oxide-sensitive guanylyl cyclase is sufficient to induce hypertension in mice, Circulation, 121, 401, 10.1161/CIRCULATIONAHA.109.890962
Friebe, 2007, Fatal gastrointestinal obstruction and hypertension in mice lacking nitric oxide-sensitive guanylyl cyclase, Proc. Natl. Acad. Sci. U.S.A., 104, 7699, 10.1073/pnas.0609778104
Erdmann, 2013, Dysfunctional nitric oxide signalling increases risk of myocardial infarction, Nature, 504, 432, 10.1038/nature12722
Erdmann, 2013, Cinaciguat, a soluble guanylate cyclase activator, unloads the heart but also causes hypotension in acute decompensated heart failure, Eur. Heart J., 34, 57, 10.1093/eurheartj/ehs196
Pfeifer, 1998, Defective smooth muscle regulation in cGMP kinase I-deficient mice, EMBO J., 17, 3045, 10.1093/emboj/17.11.3045
Michael, 2008, High blood pressure arising from a defect in vascular function, Proc. Natl. Acad. Sci. U.S.A., 105, 6702, 10.1073/pnas.0802128105
Blanton, 2013, Mutation of the protein kinase I alpha leucine zipper domain produces hypertension and progressive left ventricular hypertrophy: a novel mouse model of age-dependent hypertensive heart disease, J. Gerontol. A: Biol. Sci. Med. Sci., 68, 1351, 10.1093/gerona/glt042
Guo, 2013, Recurrent gain-of-function mutation in PRKG1 causes thoracic aortic aneurysms and acute aortic dissections, Am. J. Hum. Genet., 93, 398, 10.1016/j.ajhg.2013.06.019
Weber, 2007, Rescue of cGMP kinase I knockout mice by smooth muscle specific expression of either isozyme, Circ. Res., 101, 1096, 10.1161/CIRCRESAHA.107.154351
Loga, 2013, The role of cGMP/cGKI signalling and Trpc channels in regulation of vascular tone, Cardiovasc. Res., 100, 280, 10.1093/cvr/cvt176
Patrucco, 2011, cGMP kinase I, cardiac hypertrophy and PDE inhibition, BMC Pharmacol., 11, O19, 10.1186/1471-2210-11-S1-O19
Leiss, 2011, Cyclic GMP kinase I modulates glucagon release from pancreatic alpha-cells, Diabetes, 60, 148, 10.2337/db10-0595
Foller, 2008, Anemia and splenomegaly in cGKI-deficient mice, Proc. Natl. Acad. Sci. U.S.A., 105, 6771, 10.1073/pnas.0708940105
Takimoto, 2005, Chronic inhibition of cyclic GMP phosphodiesterase 5A prevents and reverses cardiac hypertrophy, Nat. Med., 11, 214, 10.1038/nm1175
Klaiber, 2010, Novel insights into the mechanisms mediating the local antihypertrophic effects of cardiac atrial natriuretic peptide: role of cGMP-dependent protein kinase and RGS2, Basic Res. Cardiol., 105, 583, 10.1007/s00395-010-0098-z
Takimoto, 2009, Regulator of G protein signaling 2 mediates cardiac compensation to pressure overload and antihypertrophic effects of PDE5 inhibition in mice, J. Clin. Invest., 119, 408
Takimoto, 2005, cGMP catabolism by phosphodiesterase 5A regulates cardiac adrenergic stimulation by NOS3-dependent mechanism, Circ. Res., 96, 100, 10.1161/01.RES.0000152262.22968.72
Hsu, 2009, Phosphodiesterase 5 inhibition blocks pressure overload-induced cardiac hypertrophy independent of the calcineurin pathway, Cardiovasc. Res., 81, 301, 10.1093/cvr/cvn324
Nagendran, 2007, Phosphodiesterase type 5 is highly expressed in the hypertrophied human right ventricle, and acute inhibition of phosphodiesterase type 5 improves contractility, Circulation, 116, 238, 10.1161/CIRCULATIONAHA.106.655266
Kukreja, 2012, Cyclic guanosine monophosphate signaling and phosphodiesterase-5 inhibitors in cardioprotection, J. Am. Coll. Cardiol., 59, 1921, 10.1016/j.jacc.2011.09.086
Das, 2009, ERK phosphorylation mediates sildenafil-induced myocardial protection against ischemia–reperfusion injury in mice, Am. J. Physiol. Heart Circ. Physiol., 296, H1236, 10.1152/ajpheart.00100.2009
Madhani, 2010, Phospholemman Ser69 phosphorylation contributes to sildenafil-induced cardioprotection against reperfusion injury, Am. J. Physiol. Heart Circ. Physiol., 299, H827, 10.1152/ajpheart.00129.2010
Koka, 2013, Phosphodiesterase-5 inhibitor tadalafil attenuates oxidative stress and protects against myocardial ischemia/reperfusion injury in type 2 diabetic mice, Free Radic. Biol. Med., 60, 80, 10.1016/j.freeradbiomed.2013.01.031
Koitabashi, 2010, Cyclic GMP/PKG-dependent inhibition of TRPC6 channel activity and expression negatively regulates cardiomyocyte NFAT activation. Novel mechanism of cardiac stress modulation by PDE5 inhibition, J. Mol. Cell. Cardiol., 48, 713, 10.1016/j.yjmcc.2009.11.015
Nishida, 2010, Phosphorylation of TRPC6 channels at Thr69 is required for anti-hypertrophic effects of phosphodiesterase 5 inhibition, J. Biol. Chem., 285, 13244, 10.1074/jbc.M109.074104
Takimoto, 2007, Compartmentalization of cardiac beta-adrenergic inotropy modulation by phosphodiesterase type 5, Circulation, 115, 2159, 10.1161/CIRCULATIONAHA.106.643536
Zaccolo, 2007, cAMP and cGMP signaling cross-talk: role of phosphodiesterases and implications for cardiac pathophysiology, Circ. Res., 100, 1569, 10.1161/CIRCRESAHA.106.144501
Rybalkin, 2013, Differential effects of PDE5 inhibitors on cardiac dysfunction in the MDX [m]ouse model of Duchenne muscular dystrophy, BMC Pharmacol. Toxicol., 14, O38, 10.1186/2050-6511-14-S1-O38
Pokreisz, 2009, Ventricular phosphodiesterase-5 expression is increased in patients with advanced heart failure and contributes to adverse ventricular remodeling after myocardial infarction in mice, Circulation, 119, 408, 10.1161/CIRCULATIONAHA.108.822072
Shan, 2012, Differential expression of PDE5 in failing and nonfailing human myocardium, Circ. Heart Fail., 5, 79, 10.1161/CIRCHEARTFAILURE.111.961706
Zhang, 2008, Expression, activity, and pro-hypertrophic effects of PDE5A in cardiac myocytes, Cell. Signal., 20, 2231, 10.1016/j.cellsig.2008.08.012
Vandeput, 2009, cGMP-hydrolytic activity and its inhibition by sildenafil in normal and failing human and mouse myocardium, J. Pharmacol. Exp. Ther., 330, 884, 10.1124/jpet.109.154468
Salloum, 2009, Phosphodiesterase-5 inhibitor, tadalafil, protects against myocardial ischemia/reperfusion through protein-kinase G-dependent generation of hydrogen sulfide, Circulation, 120, S31, 10.1161/CIRCULATIONAHA.108.843979
Jin, 2013, The beneficial effects of tadalafil on left ventricular dysfunction in doxorubicin-induced cardiomyopathy, J. Cardiol., 62, 110, 10.1016/j.jjcc.2013.03.018
Wehling-Henricks, 2005, Cardiomyopathy in dystrophin-deficient hearts is prevented by expression of a neuronal nitric oxide synthase transgene in the myocardium, Hum. Mol. Genet., 14, 1921, 10.1093/hmg/ddi197
Khairallah, 2008, Sildenafil and cardiomyocyte-specific cGMP signaling prevent cardiomyopathic changes associated with dystrophin deficiency, Proc. Natl. Acad. Sci. U.S.A., 105, 7028, 10.1073/pnas.0710595105
Burelle, 2010, Alterations in mitochondrial function as a harbinger of cardiomyopathy: lessons from the dystrophic heart, J. Mol. Cell. Cardiol., 48, 310, 10.1016/j.yjmcc.2009.09.004
Barst, 2012, Survival in childhood pulmonary arterial hypertension: insights from the registry to evaluate early and long-term pulmonary arterial hypertension disease management, Circulation, 125, 113, 10.1161/CIRCULATIONAHA.111.026591
Santos, 2014, Tadalafil-induced improvement in left ventricular diastolic function in resistant hypertension, Eur. J. Clin. Pharmacol., 70, 147, 10.1007/s00228-013-1611-8
Elrod, 2007, Sildenafil-mediated acute cardioprotection is independent of the NO/cGMP pathway, Am. J. Physiol. Heart Circ. Physiol., 292, H342, 10.1152/ajpheart.00306.2006
Miller, 2011, Cyclic nucleotide phosphodiesterase 1A: a key regulator of cardiac fibroblast activation and extracellular matrix remodeling in the heart, Basic Res. Cardiol., 106, 1023, 10.1007/s00395-011-0228-2
Miller, 2009, Role of Ca2+/calmodulin-stimulated cyclic nucleotide phosphodiesterase 1 in mediating cardiomyocyte hypertrophy, Circ. Res., 105, 956, 10.1161/CIRCRESAHA.109.198515
MacFarland, 1991, High concentrations of a cGMP-stimulated phosphodiesterase mediate ANP-induced decreases in cAMP and steroidogenesis in adrenal glomerulosa cells, J. Biol. Chem., 266, 136, 10.1016/S0021-9258(18)52413-3
Mehel, 2013, Phosphodiesterase-2 is up-regulated in human failing hearts and blunts beta-adrenergic responses in cardiomyocytes, J. Am. Coll. Cardiol., 62, 1596, 10.1016/j.jacc.2013.05.057
Moltzau, 2014, Differential regulation of C-type natriuretic peptide-induced cGMP and functional responses by PDE2 and PDE3 in failing myocardium, Naunyn Schmiedeberg Arch. Pharmacol., 387, 407, 10.1007/s00210-013-0953-1
Prysyazhna, 2012, Single atom substitution in mouse protein kinase G eliminates oxidant sensing to cause hypertension, Nat. Med., 18, 286, 10.1038/nm.2603
Dostmann, W. et al. The University of Vermont and State Agricultural College. Novel peptidic activators of type I cGMP dependent protein kinases and uses thereof, US20140037547
Castro, 2010, Feedback control through cGMP-dependent protein kinase contributes to differential regulation and compartmentation of cGMP in rat cardiac myocytes, Circ. Res., 107, 1232, 10.1161/CIRCRESAHA.110.226712
Mokni, 2010, Concerted regulation of cGMP and cAMP phosphodiesterases in early cardiac hypertrophy induced by angiotensin II, PLoS ONE, 5, e14227, 10.1371/journal.pone.0014227
Thunemann, 2013, Transgenic mice for cGMP imaging, Circ. Res., 113, 365, 10.1161/CIRCRESAHA.113.301063
Nausch, 2008, Differential patterning of cGMP in vascular smooth muscle cells revealed by single GFP-linked biosensors, Proc. Natl. Acad. Sci. U.S.A., 105, 365, 10.1073/pnas.0710387105
Korkmaz, 2009, Pharmacological activation of soluble guanylate cyclase protects the heart against ischemic injury, Circulation, 120, 677, 10.1161/CIRCULATIONAHA.109.870774
Cohen, 2010, Cardioprotective PKG-independent NO signaling at reperfusion, Am. J. Physiol. Heart Circ. Physiol., 299, H2028, 10.1152/ajpheart.00527.2010
Methner, 2013, Riociguat reduces infarct size and post-infarct heart failure in mouse hearts: insights from MRI/PET imaging, PLoS ONE, 8, e83910, 10.1371/journal.pone.0083910
Geschka, 2011, Soluble guanylate cyclase stimulation prevents fibrotic tissue remodeling and improves survival in salt-sensitive Dahl rats, PLoS ONE, 6, e21853, 10.1371/journal.pone.0021853
Schroter, 2010, Homologous desensitization of guanylyl cyclase A, the receptor for atrial natriuretic peptide, is associated with a complex phosphorylation pattern, FEBS J., 277, 2440, 10.1111/j.1742-4658.2010.07658.x
Bryan, 2002, The atrial natriuretic peptide receptor (NPR-A/GC-A) is dephosphorylated by distinct microcystin-sensitive and magnesium-dependent protein phosphatases, J. Biol. Chem., 277, 16041, 10.1074/jbc.M110626200