Expression of Concern: Increasing cardiac contractility after myocardial infarction exacerbates cardiac injury and pump dysfunction (Circulation Research (2010) 107 (800-809) DOI: 10.1161/CIRCRESAHA.110.219220);Increasing cardiac contractility after myocardial infarction exacerbates cardiac injury and pump dysfunction

Circulation Research

Volumn 107, Issue 6, 2010, Pages 800-809

  Zhang, Hongyu ^a   Chen, Xiongwen ^a   Gao, Erhe ^b   MacDonnell, Scott M ^c   Wang, Wei ^a   Kolpakov, Mikhail ^a   Nakayama, Hiroyuki ^d   Zhang, Xiaoying ^a   Jaleel, Naser ^a   Harris, David M ^e   Li, Yingxin ^a   Tang, Mingxin ^a   Berretta, Remus ^a   Leri, Annarosa ^f   Kajstura, Jan ^f   Sabri, Abdelkarim ^a   Koch, Walter J ^b   Molkentin, Jeffery D ^d   Houser, Steven R ^a  

^a TEMPLE UNIVERSITY SCHOOL OF MEDICINE   (United States)

^b THOMAS JEFFERSON UNIVERSITY   (United States)

^c BOEHRINGER INGELHEIM PHARMACEUTICALS INC   (United States)

^d CINCINNATI CHILDREN'S HOSPITAL MEDICAL CENTER   (United States)

^e DREXEL UNIVERSITY   (United States)

^f BRIGHAM AND WOMEN S HOSPITAL   (United States)

Author keywords

cardiac contractility; heart failure; myocardial infarction

Indexed keywords

CALCIUM; CALCIUM CHANNEL; CACNA1C PROTEIN, MOUSE; CALCIUM CHANNEL L TYPE;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CALCIUM TRANSPORT; CELL COUNT; CELL DEATH; CONTROLLED STUDY; HEART FAILURE; HEART FUNCTION; HEART HYPERTROPHY; HEART INFARCTION; HEART INJURY; HEART MUSCLE CONTRACTILITY; MOUSE; MUSCLE CELL; NONHUMAN; PRIORITY JOURNAL; SARCOPLASMIC RETICULUM; ANIMAL; CALCIUM SIGNALING; CELL CULTURE; COMPARATIVE STUDY; DEFICIENCY; GENETICS; HEART CONTRACTION; HEART MUSCLE CELL; METABOLISM; PATHOLOGY; PATHOPHYSIOLOGY; PHYSIOLOGY; TRANSGENIC MOUSE;

ANIMALS; CALCIUM CHANNELS, L-TYPE; CALCIUM SIGNALING; CELLS, CULTURED; MICE; MICE, TRANSGENIC; MYOCARDIAL CONTRACTION; MYOCARDIAL INFARCTION; MYOCYTES, CARDIAC;

EID: 77957285185     PISSN: 00097330     EISSN: 15244571     Source Type: Journal    
DOI: 10.1161/RES.0000000000000241     Document Type: Erratum

References (46)

1. Houser SR. Ca(2 +) signaling domains responsible for cardiac hypertrophy and arrhythmias. Circ Res. 2009;104:413-415.
2. Bers DM. Calcium cycling and signaling in cardiac myocytes. Annu Rev Physiol. 2008;70:23-49.
3. Wilkins BJ, Molkentin JD. Calcium-calcineurin signaling in the regulation of cardiac hypertrophy. Biochem Biophys Res Commun. 2004;322: 1178-1191.
4. Gomez AM, Guatimosim S, Dilly KW, Vassort G, Lederer WJ. Heart failure after myocardial infarction: Altered excitation-contraction coupling. Circulation. 2001;104:688-693.
5. Houser SR, Piacentino V III, Weisser J. Abnormalities of calcium cycling in the hypertrophied and failing heart. J Mol Cell Cardiol. 2000;32: 1595-1607.
6. Sam F, Sawyer DB, Chang DL, Eberli FR, Ngoy S, Jain M, Amin J, Apstein CS, Colucci WS. Progressive left ventricular remodeling and apoptosis late after myocardial infarction in mouse heart. Am J Physiol Heart Circ Physiol. 2000;279:H422-H428.
7. Abbate A, Biondi-Zoccai GG, Bussani R, Dobrina A, Camilot D, Feroce F, Rossiello R, Baldi F, Silvestri F, Biasucci LM, Baldi A. Increased myocardial apoptosis in patients with unfavorable left ventricular remodeling and early symptomatic post-infarction heart failure. J Am Coll Cardiol. 2003;41:753-760.
8. Nakayama H, Chen X, Baines CP, Klevitsky R, Zhang X, Zhang H, Jaleel N, Chua BH, Hewett TE, Robbins J, Houser SR, Molkentin JD. Ca2 +-and mitochondrial-dependent cardiomyocyte necrosis as a primary mediator of heart failure. J Clin Invest. 2007;117:2431-2444.
9. Gill C, Mestril R, Samali A. Losing heart: the role of apoptosis in heart disease-a novel therapeutic target? FASEB J. 2002;16:135-146.
10. Yue P, Long CS, Austin R, Chang KC, Simpson PC, Massie BM. Post-infarction heart failure in the rat is associated with distinct alterations in cardiac myocyte molecular phenotype. J Mol Cell Cardiol. 1998;30:1615-1630.
11. Naga Prasad SV, Nienaber J, Rockman HA. Beta-adrenergic axis and heart disease. Trends Genet. 2001;17:S44-S49.
12. Piacentino V III, Weber CR, Chen X, Weisser-Thomas J, Margulies KB, Bers DM, Houser SR. Cellular basis of abnormal calcium transients of failing human ventricular myocytes. Circ Res. 2003;92:651-658.
13. Choi DJ, Koch WJ, Hunter JJ, Rockman HA. Mechanism of beta-adrenergic receptor desensitization in cardiac hypertrophy is increased beta-adrenergic receptor kinase. J Biol Chem. 1997;272:17223-17229.
14. Ito K, Yan X, Tajima M, Su Z, Barry WH, Lorell BH. Contractile reserve and intracellular calcium regulation in mouse myocytes from normal and hypertrophied failing hearts. Circ Res. 2000;87:588-595.
15. Quaile MP, Rossman EI, Berretta RM, Bratinov G, Kubo H, Houser SR, Margulies KB. Reduced sarcoplasmic reticulum Ca(2 +) load mediates impaired contractile reserve in right ventricular pressure overload. J Mol Cell Cardiol. 2007;43:552-563.
16. Amidon TM, Parmley WW. Is there a role for positive inotropic agents in congestive heart failure: focus on mortality. Clin Cardiol. 1994;17: 641-647.
17. Landmesser U, Drexler H. Update on inotropic therapy in the management of acute heart failure. Curr Treat Options Cardiovasc Med. 2007;9:443-449.
18. Curfman GD. Inotropic therapy for heart failure-an unfulfilled promise. N Engl J Med. 1991;325:1509-1510.
19. Eichhorn EJ. Restoring function in failing hearts: the effects of beta blockers. Am J Med. 1998;104:163-169.
20. Reiken S, Wehrens XH, Vest JA, Barbone A, Klotz S, Mancini D, Burkhoff D, Marks AR. Beta-blockers restore calcium release channel function and improve cardiac muscle performance in human heart failure. Circulation. 2003;107:2459-2466.
21. Ferrari R, Ceconi C, Curello S, Visioli O. The neuroendocrine and sympathetic nervous system in congestive heart failure. Eur Heart J. 1998;19(Suppl F):F45-F51.
22. Shan K, Kurrelmeyer K, Seta Y, Wang F, Dibbs Z, Deswal A, Lee-Jackson D, Mann DL. The role of cytokines in disease progression in heart failure. Curr Opin Cardiol. 1997;12:218-223.
23. Engelhardt S, Hein L, Dyachenkow V, Kranias EG, Isenberg G, Lohse MJ. Altered calcium handling is critically involved in the cardiotoxic effects of chronic beta-adrenergic stimulation. Circulation. 2004;109:1154-1160.
24. Bers DM, Guo T. Calcium signaling in cardiac ventricular myocytes. Ann N Y Acad Sci. 2005;1047:86-98.
25. Nishida K, Otsu K. Cell death in heart failure. Circ J. 2008;72(Suppl A):A17-A21.
26. Chen X, Zhang X, Kubo H, Harris DM, Mills GD, Moyer J, Berretta R, Potts ST, Marsh JD, Houser SR. Ca2+ influx-induced sarcoplasmic reticulum Ca2+ overload causes mitochondrial-dependent apoptosis in ventricular myocytes. Circ Res. 2005;97:1009-1017.
27. Jaleel N, Nakayama H, Chen X, Kubo H, MacDonnell S, Zhang H, Berretta R, Robbins J, Cribbs L, Molkentin JD, Houser SR. Ca2+ influx through T-and L-type Ca2 + channels have different effects on myocyte contractility and induce unique cardiac phenotypes. Circ Res. 2008;103: 1109-1119.
28. Jugdutt BI. Remodeling of the myocardium and potential targets in the collagen degradation and synthesis pathways. Curr Drug Targets Cardiovasc Haematol Disord. 2003;3:1-30.
29. Bodi I, Mikala G, Koch SE, Akhter SA, Schwartz A. The L-type calcium channel in the heart: the beat goes on. J Clin Invest. 2005;115:3306-3317.
30. Striessnig J. Pharmacology, structure and function of cardiac L-type Ca(2 +) channels. Cell Physiol Biochem. 1999;9:242-269.
31. Miriyala J, Nguyen T, Yue DT, Colecraft HM. Role of Cavbeta subunits, and lack of functional reserve, in protein kinase A modulation of cardiac Cav1.2 channels. Circ Res. 2008;102:e54-e64.
32. Mukherjee R, Spinale FG. L-type calcium channel abundance and function with cardiac hypertrophy and failure: a review. J Mol Cell Cardiol. 1998;30:1899-1916.
33. Chen X, Piacentino V III, Furukawa S, Goldman B, Margulies KB, Houser SR. L-type Ca2+ channel density and regulation are altered in failing human ventricular myocytes and recover after support with mechanical assist devices. Circ Res. 2002;91:517-524.
34. Cheung JY, Bonventre JV, Malis CD, Leaf A. Calcium and ischemic injury. N Engl J Med. 1986;314:1670-1676.
35. Gustafsson AB, Gottlieb RA. Heart mitochondria: gates of life and death. Cardiovasc Res. 2008;77:334-343.
36. Opie LH, Commerford PJ, Gersh BJ, Pfeffer MA. Controversies in ventricular remodelling. Lancet. 2006;367:356-367.
37. Isaaz K, Ethevenot G, Admant P, Brembilla B, Pernot C. A new Doppler method of assessing left ventricular ejection force in chronic congestive heart failure. Am J Cardiol. 1989;64:81-87.
38. Pfeffer MA, Braunwald E. Ventricular remodeling after myocardial infarction. Experimental observations and clinical implications. Circulation. 1990;81:1161-1172.
39. Houser SR, Piacentino V III, Mattiello J, Weisser J, Gaughan JP. Functional properties of failing human ventricular myocytes. Trends Cardiovasc Med. 2000;10:101-107.
40. Khoynezhad A, Jalali Z, Tortolani AJ. A synopsis of research in cardiac apoptosis and its application to congestive heart failure. Tex Heart Inst J. 2007;34:352-359.
41. Gustafsson AB, Gottlieb RA. Autophagy in ischemic heart disease. Circ Res. 2009;104:150-158.
42. Kubo H, Margulies KB, Piacentino V, III, Gaughan JP, Houser SR. Patients with end-stage congestive heart failure treated with beta-adrenergic receptor antagonists have improved ventricular myocyte calcium regulatory protein abundance. Circulation. 2001;104:1012-1018.
43. Wehrens XH, Lehnart SE, Reiken S, Vest JA, Wronska A, Marks AR. Ryanodine receptor/calcium release channel PKA phosphorylation: a critical mediator of heart failure progression. Proc Natl Acad Sci\USA. 2006;103:511-518.
44. Foody JM, Farrell MH, Krumholz HM. Beta-blocker therapy in heart failure: scientific review. JAMA. 2002;287:883-889.
45. Byrne MJ, Power JM, Preovolos A, Mariani JA, Hajjar RJ, Kaye DM. Recirculating cardiac delivery of AAV2/1SERCA2a improves myo-cardial function in an experimental model of heart failure in large animals. Gene Ther. 2008;15:1550-1557.
46. Wehrens XH, Lehnart SE, Reiken S, van der Nagel R, Morales R, Sun J, Cheng Z, Deng SX, de Windt LJ, Landry DW, Marks AR. Enhancing calstabin binding to ryanodine receptors improves cardiac and skeletal muscle function in heart failure. Proc Natl Acad Sci\USA. 2005;102:9607-9612.