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Metabolic Remodelling of the Hypertrophied Heart

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Molecular Defects in Cardiovascular Disease

Abstract

The heart develops hypertrophy in response to persistent elevation in cardiac workload. Depending on the nature of the stimulus, cardiac hypertrophy can be categorized as pathologic or physiologic, each of which is accompanied by distinctly different phenotypic alterations including alterations in energy metabolism. These unique metabolic phenotypes may, in part, explain the differing functional outcomes of pathologically and physiologically hypertrophied hearts, especially notable following an ischemic stress. Thus, the mechanisms underlying remodelling in pathologic and physiologic cardiac hypertrophy have been the focus of many studies. A number of molecules including AMP-activated protein kinase, peroxisome proliferator-activated receptor-α, peroxisome proliferator-activated receptor gamma coactivator 1, protein kinase C, phosphoinositide-3 kinase/protein kinase B, and reactive oxygen species have been implicated as participating in the process of metabolic remodelling in cardiac hypertrophy.

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References

  1. Swynghedauw B. Phenotypic plasticity of adult myocardium: molecular mechanisms. J Exp Biol. 2006;209:2320–7.

    Article  PubMed  CAS  Google Scholar 

  2. Burelle Y, Wambolt RB, Grist M, et al. Regular exercise is associated with a protective metabolic phenotype in the rat heart. Am J Physiol Heart Circ Physiol. 2004;287:H1055–63.

    Article  PubMed  CAS  Google Scholar 

  3. Vincent G, Khairallah M, Bouchard B, et al. Metabolic phenotyping of the diseased rat heart using 13C-substrates and ex vivo perfusion in the working mode. Mol Cell Biochem. 2003;242:89–99.

    Article  PubMed  CAS  Google Scholar 

  4. Allard MF, Schonekess BO, Henning SL, et al. Contribution of oxidative metabolism and glycolysis to ATP production in hypertrophied hearts. Am J Physiol Heart Circ Physiol. 1994;267:H742–50.

    CAS  Google Scholar 

  5. Richey PA, Brown SP. Pathological versus physiological left ventricular hypertrophy: a review. J Sports Sci. 1998;16:129–41.

    Article  PubMed  CAS  Google Scholar 

  6. Allard MF. Energy substrate metabolism in cardiac hypertrophy. Curr Hypertens Rep. 2004;6:430–5.

    Article  PubMed  Google Scholar 

  7. Grossman W, Jones D, McLaurin LP. Wall stress and patterns of hypertrophy in the human left ventricle. J Clin Invest. 1975;56:56–64.

    Article  PubMed  CAS  Google Scholar 

  8. Taegtmeyer H. Genetics of energetics: transcriptional responses in cardiac metabolism. Ann Biomed Eng. 2000;28:871–6.

    Article  PubMed  CAS  Google Scholar 

  9. Frohlich ED, Apstein C, Chobanian AV, et al. The heart in hypertension. N Engl J Med. 1992;327:998–1008.

    Article  PubMed  CAS  Google Scholar 

  10. Gaasch WH, Zile MR, Hoshino PK, et al. Tolerance of the hypertrophic heart to ischemia. Studies in compensated and failing dog hearts with pressure overload hypertrophy. Circulation. 1990;81:1644–53.

    Article  PubMed  CAS  Google Scholar 

  11. Wambolt RB, Lopaschuk GD, Brownsey RW, et al. Dichloroacetate improves postischemic function of hypertrophied rat hearts. J Am Coll Cardiol. 2000;36:1378–85.

    Article  PubMed  CAS  Google Scholar 

  12. Kannel WB. Risk stratification in hypertension: new insights from the Framingham study. Am J Hypertens. 2000;13:3S–10.

    Article  PubMed  CAS  Google Scholar 

  13. Moore RL, Palmer BM. Exercise training and cellular adaptations of normal and diseased hearts. Exerc Sport Sci Rev. 1999;27:285–315.

    Article  PubMed  CAS  Google Scholar 

  14. Neely JR, Morgan HE. Relationship between carbohydrate and lipid metabolism and the energy balance of heart muscle. Annu Rev Physiol. 1974;36:413–57.

    Article  PubMed  CAS  Google Scholar 

  15. Saddik M, Lopaschuk GD. Myocardial triglyceride turnover and contribution to energy substrate utilization in isolated working rat hearts. J Biol Chem. 1991;266:8162–70.

    PubMed  CAS  Google Scholar 

  16. van der Vusse GJ, van Bilsen M, Glatz JF. Cardiac fatty acid uptake and transport in health and disease. Cardiovasc Res. 2000;45:279–93.

    Article  PubMed  Google Scholar 

  17. Lopaschuk GD, Belke DD, Gamble J, et al. Regulation of fatty acid oxidation in the mammalian heart in health and disease. Biochim Biophys Acta. 1994;1213:263–76.

    PubMed  CAS  Google Scholar 

  18. Henning SL, Wambolt RB, Schonekess BO, et al. Contribution of glycogen to aerobic myocardial glucose utilization. Circulation. 1996;93:1549–55.

    PubMed  CAS  Google Scholar 

  19. Stanley WC, Lopaschuk GD, Hall JL, et al. Regulation of myocardial carbohydrate metabolism under normal and ischaemic conditions. Cardiovasc Res. 1997;33:243–57.

    Article  PubMed  CAS  Google Scholar 

  20. el Alaoui-Talibi Z, Landormy S, Loireau A, et al. Fatty acid oxidation and mechanical performance of volume-overloaded rat hearts. Am J Physiol Heart Circ Physiol. 1992;262:H1068–74.

    CAS  Google Scholar 

  21. Hajri T, Ibrahimi A, Coburn CT, et al. Defective fatty acid uptake in the spontaneously hypertensive rat is a primary determinant of altered glucose metabolism, hyperinsulinemia, and myocardial hypertrophy. J Biol Chem. 2001;276:23661–6.

    Article  PubMed  CAS  Google Scholar 

  22. Schonekess BO, Brindley PG, Lopaschuk GD. Calcium regulation of glycolysis, glucose oxidation, and fatty acid oxidation in the aerobic and ischemic heart. Can J Physiol Pharmacol. 1995;73:1632–40.

    Article  PubMed  CAS  Google Scholar 

  23. Wambolt RB, Henning SL, English DR, et al. Regression of cardiac hypertrophy normalizes glucose metabolism and left ventricular function during reperfusion. J Mol Cell Cardiol. 1997;29:939–48.

    Article  PubMed  CAS  Google Scholar 

  24. Allard MF, Wambolt RB, Longnus SL, et al. Hypertrophied rat hearts are less responsive to the metabolic and functional effects of insulin. Am J Physiol Endocrinol Metab. 2000;279:E487–93.

    PubMed  CAS  Google Scholar 

  25. Saeedi R, Wambolt RB, Parsons H, et al. Gender and post-ischemic recovery of hypertrophied rat hearts. BMC Cardiovasc Disord. 2006;6:8.

    Article  PubMed  Google Scholar 

  26. Lopaschuk GD, Spafford MA, Marsh DR. Glycolysis is predominant source of myocardial ATP production immediately after birth. Am J Physiol Heart Circ Physiol. 1991;261:H1698–705.

    CAS  Google Scholar 

  27. Sambandam N, Lopaschuk GD, Brownsey RW, et al. Energy metabolism in the hypertrophied heart. Heart Fail Rev. 2002;7:161–73.

    Article  PubMed  CAS  Google Scholar 

  28. El Alaoui-Talibi Z, Guendouz A, Moravec M, et al. Control of oxidative metabolism in volume-overloaded rat hearts: effect of propionyl-L-carnitine. Am J Physiol Heart Circ Physiol. 1997;272:H1615–24.

    CAS  Google Scholar 

  29. de las Fuentes L, Herrero P, Peterson LR, et al. Myocardial fatty acid metabolism: independent predictor of left ventricular mass in hypertensive heart disease. Hypertension. 2003;41:83–7.

    Article  PubMed  CAS  Google Scholar 

  30. Anderson PG, Allard MF, Thomas GD, et al. Increased ischemic injury but decreased hypoxic injury in hypertrophied rat hearts. Circ Res. 1990;67:948–59.

    PubMed  CAS  Google Scholar 

  31. Saeedi R, Grist M, Wambolt RB, et al. Trimetazidine normalizes post-ischemic function of hypertrophied rat hearts. J Pharmacol Exp Ther. 2005;314:446–54.

    Article  PubMed  CAS  Google Scholar 

  32. Allard MF, Emanuel PG, Russell JA, et al. Preischemic glycogen reduction or glycolytic inhibition improves postischemic recovery of hypertrophied rat hearts. Am J Physiol Heart Circ Physiol. 1994;267:H66–74.

    CAS  Google Scholar 

  33. Lopaschuk GD, Wambolt RB, Barr RL. An imbalance between glycolysis and glucose oxidation is a possible explanation for the detrimental effects of high levels of fatty acids during aerobic reperfusion of ischemic hearts. J Pharmacol Exp Ther. 1993;264:135–44.

    PubMed  CAS  Google Scholar 

  34. Hata K, Takasago T, Saeki A, et al. Stunned myocardium after rapid correction of acidosis. Increased oxygen cost of contractility and the role of the Na(+)-H+ exchange system. Circ Res. 1994;74:794–805.

    PubMed  CAS  Google Scholar 

  35. Ford DA. Alterations in myocardial lipid metabolism during myocardial ischemia and reperfusion. Prog Lipid Res. 2002;41:6–26.

    Article  PubMed  CAS  Google Scholar 

  36. Korge P, Honda HM, Weiss JN. Effects of fatty acids in isolated mitochondria: implications for ischemic injury and cardioprotection. Am J Physiol Heart Circ Physiol. 2003;285:H259–69.

    PubMed  CAS  Google Scholar 

  37. Randle PJ, Garland PB, Hales CN, et al. The glucose fatty-acid cycle. Its role in insulin sensitivity and the metabolic disturbances of diabetes mellitus. Lancet. 1963;1:785–9.

    Article  PubMed  CAS  Google Scholar 

  38. Sack MN, Rader TA, Park S, et al. Fatty acid oxidation enzyme gene expression is downregulated in the failing heart. Circulation. 1996;94:2837–42.

    PubMed  CAS  Google Scholar 

  39. Iemitsu M, Miyauchi T, Maeda S, et al. Cardiac hypertrophy by hypertension and exercise training exhibits different gene expression of enzymes in energy metabolism. Hypertens Res. 2003;26:829–37.

    Article  PubMed  CAS  Google Scholar 

  40. Luiken JJ, Arumugam Y, Dyck DJ, et al. Increased rates of fatty acid uptake and plasmalemmal fatty acid transporters in obese Zucker rats. J Biol Chem. 2001;276:40567–73.

    Article  PubMed  CAS  Google Scholar 

  41. van der Vusse GJ, van Bilsen M, Glatz JF, et al. Critical steps in cellular fatty acid uptake and utilization. Mol Cell Biochem. 2002;239:9–15.

    Article  PubMed  Google Scholar 

  42. Zonderland ML, Bar PR, Reijneveld JC, et al. Different metabolic adaptation of heart and skeletal muscles to moderate-intensity treadmill training in the rat. Eur J Appl Physiol Occup Physiol. 1999;79:391–6.

    Article  PubMed  CAS  Google Scholar 

  43. Rimbaud S, Sanchez H, Garnier A, et al. Stimulus specific changes of energy metabolism in hypertrophied heart. J Mol Cell Cardiol. 2009;46:952–9.

    Article  PubMed  CAS  Google Scholar 

  44. Tian R, Musi N, D’Agostino J, et al. Increased adenosine monophosphate-activated protein kinase activity in rat hearts with pressure-overload hypertrophy. Circulation. 2001;104:1664–9.

    Article  PubMed  CAS  Google Scholar 

  45. Krishnan J, Suter M, Windak R, et al. Activation of a HIF1alpha-PPARgamma axis underlies the integration of glycolytic and lipid anabolic pathways in pathologic cardiac hypertrophy. Cell Metab. 2009;9:512–24.

    Article  PubMed  CAS  Google Scholar 

  46. Kim J, Wende AR, Sena S, et al. Insulin-like growth factor I receptor signaling is required for exercise-induced cardiac hypertrophy. Mol Endocrinol. 2008;22:2531–43.

    Article  PubMed  CAS  Google Scholar 

  47. De Sousa E, Veksler V, Minajeva A, et al. Subcellular creatine kinase alterations. Implications in heart failure. Circ Res. 1999;85:68–76.

    PubMed  Google Scholar 

  48. Kudo N, Barr AJ, Barr RL, et al. High rates of fatty acid oxidation during reperfusion of ischemic hearts are associated with a decrease in malonyl-CoA levels due to an increase in 5′-AMP-activated protein kinase inhibition of acetyl-CoA carboxylase. J Biol Chem. 1995;270:17513–20.

    Article  PubMed  CAS  Google Scholar 

  49. Hardie DG, Sakamoto K. AMPK: a key sensor of fuel and energy status in skeletal muscle. Physiology (Bethesda). 2006;21:48–60.

    CAS  Google Scholar 

  50. Carling D, Sanders MJ, Woods A. The regulation of AMP-activated protein kinase by upstream kinases. Int J Obes (Lond). 2008;32 Suppl 4:S55–9.

    Article  CAS  Google Scholar 

  51. Sakamoto K, McCarthy A, Smith D, et al. Deficiency of LKB1 in skeletal muscle prevents AMPK activation and glucose uptake during contraction. EMBO J. 2005;24:1810–20.

    Article  PubMed  CAS  Google Scholar 

  52. Woods A, Dickerson K, Heath R, et al. Ca2+/calmodulin-dependent protein kinase kinase-beta acts upstream of AMP-activated protein kinase in mammalian cells. Cell Metab. 2005;2:21–33.

    Article  PubMed  CAS  Google Scholar 

  53. Allard MF, Parsons HL, Saeedi R, et al. AMPK and metabolic adaptation by the heart to pressure overload. Am J Physiol Heart Circ Physiol. 2007;292:H140–8.

    Article  PubMed  CAS  Google Scholar 

  54. Chabowski A, Momken I, Coort S, et al. Prolonged AMPK activation increases the expression of fatty acid transporters in cardiac myocytes and perfused hearts. Mol Cell Biochem. 2006;288:201–12.

    Article  PubMed  CAS  Google Scholar 

  55. An D, Pulinilkunnil T, Qi D, et al. The metabolic “switch” AMPK regulates cardiac heparin-releasable lipoprotein lipase. Am J Physiol Endocrinol Metab. 2005;288:E246–53.

    Article  PubMed  CAS  Google Scholar 

  56. McGarry JD. Malonyl-CoA and carnitine palmitoyltransferase I: an expanding partnership. Biochem Soc Trans. 1995;23:481–5.

    PubMed  CAS  Google Scholar 

  57. Russell III RR, Bergeron R, Shulman GI, et al. Translocation of myocardial GLUT-4 and increased glucose uptake through activation of AMPK by AICAR. Am J Physiol Heart Circ Physiol. 1999;277:H643–9.

    CAS  Google Scholar 

  58. Marsin A-S, Bertrand L, Rider MH, et al. Phosphorylation and activation of heart PFK-2 by AMPK has a role in the stimulation of glycolysis during ischemia. Curr Biol. 2000;10:1247–55.

    Article  PubMed  CAS  Google Scholar 

  59. Narabayashi H, Lawson JW, Uyeda K. Regulation of phosphofructokinase in perfused rat heart. Requirement for fructose 2,6-bisphosphate and a covalent modification. J Biol Chem. 1985;260:9750–8.

    PubMed  CAS  Google Scholar 

  60. Winder WW, Holmes BF, Rubink DS, et al. Activation of AMP-activated protein kinase increases mitochondrial enzymes in skeletal muscle. J Appl Physiol. 2000;88:2219–26.

    PubMed  CAS  Google Scholar 

  61. Holmes BF, Kurth-Kraczek EJ, Winder WW. Chronic activation of 5′-AMP-activated protein kinase increases GLUT-4, hexokinase, and glycogen in muscle. J Appl Physiol. 1999;87:1990–5.

    PubMed  CAS  Google Scholar 

  62. Jorgensen SB, Richter EA, Wojtaszewski JF. Role of AMPK in skeletal muscle metabolic regulation and adaptation in relation to exercise. J Physiol. 2006;574:17–31.

    Article  PubMed  Google Scholar 

  63. Saeedi R, Saran VV, Wu SSY, et al. AMP-activated protein kinase influences metabolic remodeling in H9c2 cells hypertrophied by arginine vasopressin. Am J Physiol Heart Circ Physiol. 2009;296:H1822–32.

    Article  PubMed  CAS  Google Scholar 

  64. Musi N, Hirshman MF, Arad M, et al. Functional role of AMP-activated protein kinase in the heart during exercise. FEBS Lett. 2005;579:2045–50.

    Article  PubMed  CAS  Google Scholar 

  65. Terada S, Goto M, Kato M, et al. Effects of low-intensity prolonged exercise on PGC-1 mRNA expression in rat epitrochlearis muscle. Biochem Biophys Res Commun. 2002;296:350–4.

    Article  PubMed  CAS  Google Scholar 

  66. Burns KA, Vanden Heuvel JP. Modulation of PPAR activity via phosphorylation. Biochim Biophys Acta. 2007;1771:952–60.

    PubMed  CAS  Google Scholar 

  67. Finck BN. The PPAR regulatory system in cardiac physiology and disease. Cardiovasc Res. 2007;73:269–77.

    Article  PubMed  CAS  Google Scholar 

  68. Barger PM, Brandt JM, Leone TC, et al. Deactivation of peroxisome proliferator-activated receptor-alpha during cardiac hypertrophic growth. J Clin Invest. 2000;105:1723–30.

    Article  PubMed  CAS  Google Scholar 

  69. Lehman JJ, Kelly DP. Gene regulatory mechanisms governing energy metabolism during cardiac hypertrophic growth. Heart Fail Rev. 2002;7:175–85.

    Article  PubMed  CAS  Google Scholar 

  70. Akki A, Smith K, Seymour AM. Compensated ­cardiac hypertrophy is characterised by a decline in palmitate oxidation. Mol Cell Biochem. 2008;311:215–24.

    Article  PubMed  CAS  Google Scholar 

  71. O’Neill BT, Kim J, Wende AR, et al. A conserved role for phosphatidylinositol 3-kinase but not Akt signaling in mitochondrial adaptations that accompany physiological cardiac hypertrophy. Cell Metab. 2007;6:294–306.

    Article  PubMed  Google Scholar 

  72. Malhotra R, D’Souza KM, Staron ML, et al. Gαq-mediated activation of GRK2 by mechanical stretch in cardiac myocytes. J Biol Chem. 2010;285:13748–60.

    Article  PubMed  CAS  Google Scholar 

  73. Mayr M, Chung Y-L, Mayr U, et al. Loss of PKC-{delta} alters cardiac metabolism. Am J Physiol Heart Circ Physiol. 2004;287:H937–45.

    Article  PubMed  CAS  Google Scholar 

  74. Liu Q, Chen X, MacDonnell SM, et al. Protein kinase C{alpha}, but not PKC{beta} or PKC{gamma}, regulates contractility and heart failure susceptibility: implications for ruboxistaurin as a novel therapeutic approach. Circ Res. 2009;105:194–200.

    Article  PubMed  CAS  Google Scholar 

  75. Gu X, Bishop SP. Increased protein kinase C and isozyme redistribution in pressure-overload cardiac hypertrophy in the rat. Circ Res. 1994;75:926–31.

    PubMed  CAS  Google Scholar 

  76. Dorn II GW, Force T. Protein kinase cascades in the regulation of cardiac hypertrophy. J Clin Invest. 2005;115:527–37.

    PubMed  CAS  Google Scholar 

  77. Shiojima I, Sato K, Izumiya Y, et al. Disruption of coordinated cardiac hypertrophy and angiogenesis contributes to the transition to heart failure. J Clin Invest. 2005;115:2108–18.

    Article  PubMed  CAS  Google Scholar 

  78. McMullen JR, Shioi T, Zhang L, et al. Phosphoinositide 3-kinase(p110alpha) plays a critical role for the induction of physiological, but not pathological, cardiac hypertrophy. Proc Natl Acad Sci USA. 2003;100:12355–60.

    Article  PubMed  CAS  Google Scholar 

  79. Patrucco E, Notte A, Barberis L, et al. PI3Kgamma modulates the cardiac response to chronic pressure overload by distinct kinase-dependent and -independent effects. Cell. 2004;118:375–87.

    Article  PubMed  CAS  Google Scholar 

  80. Condorelli G, Drusco A, Stassi G, et al. Akt induces enhanced myocardial contractility and cell size in vivo in transgenic mice. Proc Natl Acad Sci USA. 2002;99:12333–8.

    Article  PubMed  CAS  Google Scholar 

  81. Matsui T, Li L, Wu JC, et al. Phenotypic spectrum caused by transgenic overexpression of activated Akt in the heart. J Biol Chem. 2002;277:22896–901.

    Article  PubMed  CAS  Google Scholar 

  82. DeBosch B, Treskov I, Lupu TS, et al. Akt1 is required for physiological cardiac growth. Circulation. 2006;113:2097–104.

    Article  PubMed  CAS  Google Scholar 

  83. DeBosch B, Sambandam N, Weinheimer C, et al. Akt2 regulates cardiac metabolism and cardiomyocyte survival. J Biol Chem. 2006;281:32841–51.

    Article  PubMed  CAS  Google Scholar 

  84. Proud CG. Ras, PI3-kinase and mTOR signaling in cardiac hypertrophy. Cardiovasc Res. 2004;63:403–13.

    Article  PubMed  CAS  Google Scholar 

  85. Kim CH, Cho YS, Chun YS, et al. Early expression of myocardial HIF-1alpha in response to mechanical stresses: regulation by stretch-activated channels and the phosphatidylinositol 3-kinase signaling pathway. Circ Res. 2002;90:E25–33.

    Article  PubMed  CAS  Google Scholar 

  86. Semenza GL, Roth PH, Fang HM, et al. Transcriptional regulation of genes encoding glycolytic enzymes by hypoxia-inducible factor 1. J Biol Chem. 1994;269:23757–63.

    PubMed  CAS  Google Scholar 

  87. Xue W, Cai L, Tan Y, et al. Cardiac-specific overexpression of HIF-1{alpha} prevents deterioration of glycolytic pathway and cardiac remodeling in streptozotocin-induced diabetic mice. Am J Pathol. 2010;177:97–105.

    Article  PubMed  CAS  Google Scholar 

  88. Shyu KG, Liou JY, Wang BW. Carvedilol prevents cardiac hypertrophy and overexpression of hypoxia-inducible factor-1alpha and vascular endothelial growth factor in pressure-overloaded rat heart. J Biomed Sci. 2005;12:409–20.

    Article  PubMed  CAS  Google Scholar 

  89. Luo J, McMullen JR, Sobkiw CL, et al. Class IA phosphoinositide 3-kinase regulates heart size and physiological cardiac hypertrophy. Mol Cell Biol. 2005;25:9491–502.

    Article  PubMed  CAS  Google Scholar 

  90. Ritchie RH, Delbridge LM. Cardiac hypertrophy, substrate utilization and metabolic remodelling: cause or effect? Clin Exp Pharmacol Physiol. 2006;33:159–66.

    Article  PubMed  CAS  Google Scholar 

  91. Sauer H, Wartenberg M. Reactive oxygen species as signaling molecules in cardiovascular differentiation of embryonic stem cells and tumor-induced angiogenesis. Antioxid Redox Signal. 2005;7:1423–34.

    Article  PubMed  CAS  Google Scholar 

  92. Tsutsui H, Kinugawa S, Matsushima S. Mitochondrial oxidative stress and dysfunction in myocardial remodelling. Cardiovasc Res. 2009;81:449–56.

    Article  PubMed  CAS  Google Scholar 

  93. Akki A, Zhang M, Murdoch C, et al. NADPH oxidase signaling and cardiac myocyte function. J Mol Cell Cardiol. 2009;47:15–22.

    Article  PubMed  CAS  Google Scholar 

  94. Dolinsky VW, Chan AYM, Robillard Frayne I, et al. Resveratrol prevents the prohypertrophic effects of oxidative stress on LKB1. Circulation. 2009;119:1643–52.

    Article  PubMed  CAS  Google Scholar 

  95. Nakamura K, Fushimi K, Kouchi H, et al. Inhibitory effects of antioxidants on neonatal rat cardiac myocyte hypertrophy induced by tumor necrosis factor-alpha and angiotensin II. Circulation. 1998;98:794–9.

    PubMed  CAS  Google Scholar 

  96. Kong SW, Bodyak N, Yue P, et al. Genetic expression profiles during physiological and pathological cardiac hypertrophy and heart failure in rats. Physiol Genomics. 2005;21:34–42.

    Article  PubMed  CAS  Google Scholar 

  97. Mialet-Perez J, Bianchi P, Kunduzova O, et al. New insights on receptor-dependent and monoamine oxidase-dependent effects of serotonin in the heart. J Neural Transm. 2007;114:823–7.

    Article  PubMed  CAS  Google Scholar 

  98. Fischer Y, Thomas J, Kamp J, et al. 5-Hydroxytryptamine stimulates glucose transport in cardiomyocytes via a monoamine oxidase-dependent reaction. Biochem J. 1995;311:575–83.

    PubMed  CAS  Google Scholar 

  99. Li JM, Gall NP, Grieve DJ, et al. Activation of NADPH oxidase during progression of cardiac hypertrophy to failure. Hypertension. 2002;40:477–84.

    Article  PubMed  CAS  Google Scholar 

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Acknowledgements

This work was supported by CIHR. We thank Mr. Rich Wambolt and all the current and former members of the Allard laboratory who have contributed to the studies summarized here.

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Correspondence to Michael F. Allard .

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Dai, J.M., Allard, M.F. (2011). Metabolic Remodelling of the Hypertrophied Heart. In: Dhalla, N., Nagano, M., Ostadal, B. (eds) Molecular Defects in Cardiovascular Disease. Springer, New York, NY. https://doi.org/10.1007/978-1-4419-7130-2_10

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