Cardiomyocyte Ca2+ dynamics: clinical perspectives

Scandinavian Cardiovascular Journal

Volumn 50, Issue 2, 2016, Pages 65-77

  Aronsen, Jan Magnus ^a   Louch, William E ^b   Sjaastad, Ivar ^b  

^a BJØRKNES UNIVERSITY COLLEGE   (Norway)

^b ULLEVÅL UNIVERSITY HOSPITAL   (Norway)

Author keywords

Calcium; cardiomyocyte; pathophysiology

Indexed keywords

BETA ADRENERGIC RECEPTOR BLOCKING AGENT; CALCINEURIN; CALCIUM; CALCIUM CHANNEL BLOCKING AGENT; CARDIAC GLYCOSIDE; CYCLIC AMP; CYCLIC AMP DEPENDENT PROTEIN KINASE; ENKEPHALINASE INHIBITOR; HISTONE DEACETYLASE; INOTROPIC AGENT; NATRIURETIC FACTOR; NITRIC ACID DERIVATIVE; NITRIC OXIDE DONOR; NITROGEN OXIDE; PROTEIN; RYANODINE RECEPTOR; SERCA2 PROTEIN; TRANSCRIPTION FACTOR NFAT; UNCLASSIFIED DRUG; CARDIOVASCULAR AGENT;

ADRENERGIC SYSTEM; ANAEROBIC GLYCOLYSIS; ARRHYTHMOGENESIS; CALCIUM BALANCE; CALCIUM HOMEOSTASIS; CALCIUM TRANSPORT; CARDIAC MUSCLE CELL; GENETIC TRANSCRIPTION; HEART ARRHYTHMIA; HEART DISEASE; HEART FAILURE; HEART VENTRICLE HYPERTROPHY; ISCHEMIC HEART DISEASE; MEMBRANE DEPOLARIZATION; MITOCHONDRION; MYOFILAMENT; NEGATIVE FEEDBACK; PATHOPHYSIOLOGY; PRIORITY JOURNAL; PROTEIN DEGRADATION; REPERFUSION INJURY; REVIEW; RNA TRANSLATION; SARCOPLASMIC RETICULUM; SIGNAL TRANSDUCTION; SODIUM BALANCE; ACTION POTENTIAL; ANIMAL; CALCIUM SIGNALING; DRUG EFFECTS; EXCITATION CONTRACTION COUPLING; HEART CONTRACTION; HEART DISEASES; HUMAN; KINETICS; METABOLISM;

ACTION POTENTIALS; ANIMALS; CALCIUM; CALCIUM SIGNALING; CARDIOVASCULAR AGENTS; EXCITATION CONTRACTION COUPLING; HEART DISEASES; HUMANS; KINETICS; MYOCARDIAL CONTRACTION; MYOCYTES, CARDIAC;

EID: 84958045601     PISSN: 14017431     EISSN: 16512006     Source Type: Journal    
DOI: 10.3109/14017431.2015.1136079     Document Type: Review

References (74)

1. D.M.Bers Cardiac excitation-contraction coupling. Nature. 2002;415:198–205.
2. G.S.Williams, L.Boyman, A.C.Chikando, et al. Mitochondrial calcium uptake. Proc Natl Acad Sci USA. 2013;110:10479–10486.
3. J.Q.Kwong, J.D.Molkentin Physiological and pathological roles of the mitochondrial permeability transition pore in the heart. Cell Metab. 2015;21:206–214.
4. 2+ in a cardiac myocyte. J Mol Cell Cardiol. 2012;52:317–322.
5. D.Eisner, E.Bode, L.Venetucci, et al. Calcium flux balance in the heart. J Mol Cell Cardiol. 2013;58:110–117.
6. I.Sjaastad, I.Schiander, A.Sjetnan, et al. Increased contribution of alpha 1- vs. beta-adrenoceptor-mediated inotropic response in rats with congestive heart failure. Acta Physiol Scand. 2003;177:449–458.
7. R.M.Saraiva, J.M.Hare Nitric oxide signaling in the cardiovascular system: implications for heart failure. Curr Opin Cardiol. 2006;21:221–228.
8. 2+ current in single heart cells. Nature. 1986;323:273–275.
9. L.R.Moltzau, J.M.Aronsen, S.Meier, et al. Different compartmentation of responses to brain natriuretic peptide and C-type natriuretic peptide in failing rat ventricle. J Pharmacol Exp Ther. 2014;350:681–690.
10. L.R.Moltzau, J.M.Aronsen, S.Meier, et al. SERCA2 activity is involved in the CNP-mediated functional responses in failing rat myocardium. Br J Pharmacol. 2013;170:366–379.
11. E.Qvigstad, L.R.Moltzau, J.M.Aronsen, et al. Natriuretic peptides increase beta1-adrenoceptor signalling in failing hearts through phosphodiesterase 3 inhibition. Cardiovasc Res. 2010;85:763–772.
12. K.Tasken, E.M.Aandahl Localized effects of cAMP mediated by distinct routes of protein kinase A. Physiol Rev. 2004;84:137–167.
13. C.B.Nichols, C.F.Rossow, M.F.Navedo, et al. Sympathetic stimulation of adult cardiomyocytes requires association of AKAP5 with a subpopulation of L-type calcium channels. Circ Res. 2010;107:747–756.
14. J.R.Erickson, L.Pereira, L.Wang, et al. Diabetic hyperglycaemia activates CaMKII and arrhythmias by O-linked glycosylation. Nature. 2013;502:372–376.
15. 2+ re-uptake into heart sarcoplasmic reticulum. EMBO Rep. 2007;8:1061–1067.
16. S.Beca, F.Ahmad, W.Shen, et al. Phosphodiesterase type 3A regulates basal myocardial contractility through interacting with sarcoplasmic reticulum calcium ATPase type 2a signaling complexes in mouse heart. Circ Res. 2013;112:289–297.
17. 2+ current. Circ Res. 2011;109:1024–1030.
18. A.Singh, J.M.Redden, M.S.Kapiloff, et al. The large isoforms of A-kinase anchoring protein 18 mediate the phosphorylation of inhibitor-1 by protein kinase A and the inhibition of protein phosphatase 1 activity. Mol Pharmacol. 2011;79:533–540.
19. P.J.Mohler, J.J.Schott, A.O.Gramolini, et al. Ankyrin-B mutation causes type 4 long-QT cardiac arrhythmia and sudden cardiac death. Nature. 2003;421:634–639.
20. J.M.Aronsen, F.Swift, O.M.Sejersted Cardiac sodium transport and excitation-contraction coupling. J Mol Cell Cardiol. 2013;61:11–19.
21. 2+ release in cardiomyocytes. Biophys J. 2006;91:779–792.
22. 2+ uptake during excitation-contraction coupling and impairs energetic adaptation in cardiac myocytes. Circ Res. 2006;99:172–182.
23. +-ATPase alpha2-isoform in heart failure. Cardiovasc Res. 2008;78:71–78.
24. 2 activity. J Physiol. 2015;593:1509–1521.
25. P.Han, W.Li, C.H.Lin, et al. A long noncoding RNA protects the heart from pathological hypertrophy. Nature. 2014;514:102–106.
26. C.Wahlquist, D.Jeong, A.Rojas-Munoz, et al. Inhibition of miR-25 improves cardiac contractility in the failing heart. Nature. 2014;508:531–535.
27. C.Kho, A.Lee, D.Jeong, et al. SUMO1-dependent modulation of SERCA2a in heart failure. Nature. 2011;477:601–605.
28. L.A.Venetucci, A.W.Trafford, S.C.O'Neill, et al. The sarcoplasmic reticulum and arrhythmogenic calcium release. Cardiovasc Res. 2008;77:285–292.
29. B.M.Dumotier A straightforward guide to the basic science behind arrhythmogenesis. Heart. 2014;100:1907–1915.
30. M.Harada, X.Luo, X.Y.Qi, et al. Transient receptor potential canonical-3 channel-dependent fibroblast regulation in atrial fibrillation. Circulation. 2012;126:2051–2064.
31. D.J.Hausenloy, D.M.Yellon Myocardial ischemia-reperfusion injury: a neglected therapeutic target. J Clin Invest. 2013;123:92–100.
32. H.S.Silverman, M.D.Stern Ionic basis of ischaemic cardiac injury: insights from cellular studies. Cardiovasc Res. 1994;28:581–597.
33. E.Murphy, C.Steenbergen Mechanisms underlying acute protection from cardiac ischemia-reperfusion injury. Physiol Rev. 2008;88:581–609.
34. H.M.Piper The calcium paradox revisited: an artefact of great heuristic value. Cardiovasc Res. 2000;45:123–127.
35. W.E.Louch, G.R.Ferrier, S.E.Howlett Changes in excitation-contraction coupling in an isolated ventricular myocyte model of cardiac stunning. Am J Physiol Heart Circ Physiol. 2002;283:H800–H810.
36. 2+ exchange by KB-R7943: transport mode selectivity and antiarrhythmic consequences. Am J Physiol Heart Circ Physiol. 2001;281:H1334–H1345.
37. E.F.du Toit, L.H.Opie Antiarrhythmic properties of specific inhibitors of sarcoplasmic reticulum calcium ATPase in the isolated perfused rat heart after coronary artery ligation. J Am Coll Cardiol. 1994;23:1505–1510.
38. D.M.Yellon, D.J.Hausenloy Myocardial reperfusion injury. N Engl J Med. 2007;357:1121–1135.
39. R.Bolli, E.Marban Molecular and cellular mechanisms of myocardial stunning. Physiol Rev. 1999;79:609–634.
40. W.E.Louch, G.R.Ferrier, S.E.Howlett Losartan improves recovery of contraction and inhibits transient inward current in a cellular model of cardiac ischemia and reperfusion. J Pharmacol Exp Ther. 2000;295:697–704.
41. N.Frey, E.N.Olson Cardiac hypertrophy: the good, the bad, and the ugly. Annu Rev Physiol. 2003;65:45–79.
42. J.Heineke, J.D.Molkentin Regulation of cardiac hypertrophy by intracellular signalling pathways. Nat Rev Mol Cell Biol. 2006;7:589–600.
43. A.V.Finsen, I.G.Lunde, I.Sjaastad, et al. Syndecan-4 is essential for development of concentric myocardial hypertrophy via stretch-induced activation of the calcineurin-NFAT pathway. PLoS One. 2011;6:e28302.
44. 2+-dependent hypertrophic signaling. Am J Physiol Heart Circ Physiol. 2012;302:H2574–H2582.
45. A.Zoccarato, N.C.Surdo, J.M.Aronsen, et al. Cardiac Hypertrophy Is Inhibited by a Local Pool of cAMP Regulated by Phosphodiesterase 2. Circ Res. 2015;117:707–719.
46. J.Backs, E.N.Olson Control of cardiac growth by histone acetylation/deacetylation. Circ Res. 2006;98:15–24.
47. 2+ signaling in cardiac myocyte excitation-transcription coupling. J Clin Invest. 2006;116:675–682.
48. F.M.Drawnel, D.Wachten, J.D.Molkentin, et al. Mutual antagonism between IP(3)RII and miRNA-133a regulates calcium signals and cardiac hypertrophy. J Cell Biol. 2012;199:783–798.
49. J.Bokenes, J.M.Aronsen, J.A.Birkeland, et al. Slow contractions characterize failing rat hearts. Basic Res Cardiol. 2008;103:328–344.
50. 2+ release and contraction during heart failure progression in postinfarction mice. Am J Physiol Heart Circ Physiol. 2009;296:H1069–H1079.
51. 2+ handling. J Biomed Biotechnol. 2010;2010:503906
52. 2+ release in myocytes from chronically ischemic myocardium. Circ Res. 2008;102:338–346.
53. 2+ release in murine cardiomyocytes following myocardial infarction. J Physiol (Lond). 2006;574:519–533.
54. L.Oyehaug, K.O.Loose, G.F.Jolle, et al. Synchrony of cardiomyocyte Ca(2+) release is controlled by T-tubule organization, SR Ca(2+) content, and ryanodine receptor Ca(2+) sensitivity. Biophys J. 2013;104:1685–1697.
55. 2+ release by action potential configuration in normal and failing murine cardiomyocytes. Biophys J. 2010;99:1377–1386.
56. 2+ release units? J Mol Cell Cardiol. 2013;58:41–52.
57. S.J.Briston, J.L.Caldwell, M.A.Horn, et al. Impaired beta-adrenergic responsiveness accentuates dysfunctional excitation-contraction coupling in an ovine model of tachypacing-induced heart failure. J Physiol. 2011;589:1367–1382.
58. J.O.Mudd, D.A.Kass Tackling heart failure in the twenty-first century. Nature. 2008;451:919–928.
59. W.E.Louch, M.K.Stokke, I.Sjaastad, et al. No rest for the weary: diastolic calcium homeostasis in the normal and failing myocardium. Physiology (Bethesda). 2012;27:308–323.
60. W.E.Louch, K.Hougen, H.K.Mork, et al. Sodium accumulation promotes diastolic dysfunction in end-stage heart failure following Serca2 knockout. J Physiol (Lond). 2010;588:465–478.
61. W.A.Linke, N.Hamdani Gigantic business: titin properties and function through thick and thin. Circ Res. 2014;114:1052–1068.
62. D.Westermann, D.Lindner, M.Kasner, et al. Cardiac inflammation contributes to changes in the extracellular matrix in patients with heart failure and normal ejection fraction. Circ Heart Fail. 2011;4:44–52.
63. K.M.Herum, I.G.Lunde, B.Skrbic, et al. Syndecan-4 signaling via NFAT regulates extracellular matrix production and cardiac myofibroblast differentiation in response to mechanical stress. J Mol Cell Cardiol. 2013;54:73–81.
64. K.M.Herum, I.G.Lunde, B.Skrbic, et al. Syndecan-4 is a key determinant of collagen cross-linking and passive myocardial stiffness in the pressure-overloaded heart. Cardiovasc Res. 2015;106:217–226.
65. S.M.Pogwizd, K.Schlotthauer, L.Li, et al. Arrhythmogenesis and contractile dysfunction in heart failure: roles of sodium-calcium exchange, inward rectifier potassium current, and residual beta-adrenergic responsiveness. Circ Res. 2001;88:1159–1167.
66. 2+ wave development in ventricular myocytes. Cardiovasc Res. 2010;86:63–71.
67. M.K.Stokke, S.J.Briston, G.F.Jolle, et al. Ca(2+) wave probability is determined by the balance between SERCA2-dependent Ca(2+) reuptake and threshold SR Ca(2+) content. Cardiovasc Res. 2011;90:503–512.
68. R.S.Foo, K.Mani, R.N.Kitsis Death begets failure in the heart. J Clin Invest. 2005;115:565–571.
69. 2+ homeostasis in heart failure. Curr Pharm Des. 2015;21:431–448.
70. M.K.Stokke, N.Tovsrud, W.E.Louch, et al. I(CaL) inhibition prevents arrhythmogenic Ca(2+) waves caused by abnormal Ca(2+) sensitivity of RyR or SR Ca(2+) accumulation. Cardiovasc Res. 2013;98:315–325.
71. J.J.McMurray, M.Packer, A.S.Desai, et al. Angiotensin-neprilysin inhibition versus enalapril in heart failure. N Engl J Med. 2014;371:993–1004.
72. 2+-ATPase in patients with advanced heart failure. Circulation. 2011;124:304–313. %19;
73. B.Lygren, K.Tasken The potential use of AKAP18delta as a drug target in heart failure patients. Expert Opin Biol Ther. 2008;8:1099–1108.
74. A.H.Ottesen, W.E.Louch, C.R.Carlson, et al. Secretoneurin is a novel prognostic cardiovascular biomarker associated with cardiomyocyte calcium handling. J Am Coll Cardiol. 2015;65:339–351.